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Journal articles on the topic 'Molecular aspects of Autoimmune diseases'
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1
Lepage, V., L. U. Lamm, and D. Charron. "MOLECULAR ASPECTS OF HLA CLASS II AND SOME AUTOIMMUNE DISEASES." European Journal of Immunogenetics 20, no. 3 (June 1993): 153–64. http://dx.doi.org/10.1111/j.1744-313x.1993.tb00106.x.
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PAPADOGIANNAKIS (E. Ι. ΠΑΠΑΔΟΓΙΑΝΝΑΚΗΣ), E. M. "Contemporary aspects on the immunopathogenesis of pemphigus group in the dog." Journal of the Hellenic Veterinary Medical Society 55, no. 4 (December 6, 2017): 319. http://dx.doi.org/10.12681/jhvms.15128.
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Autoimmune diseases of the canine epidermis originate from the activation of the immune system against some adhesion molecules, which link the keratinocytes. Epidermal autoimmunity eventually induces acantholysis, which is thepathological hallmark of these skin diseases. In this review article, a thorough analysis of the immunopathogenesis for each of these skin diseases has been attempted along with the mechanisms that modulate the process of acantholysis. Epidermal autoimmune diseases in the dog include pemphigus foliaceus, vulgaris, panepidermal pustular, erythematosus, paraneoplastic and pharmaceutical. The recent advances in immunopathological and molecular techniques have markedly facilitated the understanding of their pathogenesis, thus giving the opportunity for the development of new therapeutic strategies that may lead to their successful treatment.
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Nassonov, Eugeney L., Mikhail Y. Samsonov, Barbara Wirleitner, Gernot P. Tilz, and Dietmar Fuchs. "Neopterin in Autoimmune Rheumatic Diseases." Pteridines 10, no. 3 (August 1999): 119–24. http://dx.doi.org/10.1515/pteridines.1999.10.3.119.
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Abstract Neopterin concentrations in body fluids allow to monitor the activation status of the cellular ( =Thl-type) llnmune system in an easy but also sensitive way. Autoimmune disease result from deterioration of almost .1,1 immune system compartments. Rheumatic disorders comprise an important group of diseases featuring several aspects of autoimmune disorders. Already several years ago increased neopterin concentrations were Jemonstrated in patients with rheumatoid arthritis and later on in patients with systemic lupus erythemarosus. Neopterin concentrations were fowld to correlate with the activity of the diseases and to conveniently indicate effects of therapy. Similar data were obtained in patients with acute rheumatic fever, and more recently, the utility of neopterin determination was also demonstrated in patients with Wegeners granulomatosis and with polymytositis/dermatomyositis. In this article we intend to summarize the current knowledge about the usefulness of neopterin measurements in patients with rheumatic diseases.
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Chetina, E. V., and E. P. Sharapova. "Rheumatic pain management: molecular aspects." Modern Rheumatology Journal 14, no. 1 (March 22, 2020): 93–100. http://dx.doi.org/10.14412/1996-7012-2020-1-93-100.
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Rheumatic diseases (RDs), including osteoarthritis and rheumatoid arthritis, are non-infectious slowly progressive incurable inflammatory diseases that lead to prolonged disability due to damage to the musculoskeletal system. Pain is a dominant symptom at any stage of these diseases, is directly related to joint functioning, and determines the quality of life in patients. Moreover, despite the significant successes of studying the role of inflammation and regulation of autoimmune processes, the pathogenetic mechanisms for the development and maintenance of pain in RDs are little investigated. The nociceptive mechanisms due to inflammation and/or joint structural impairment are involved in the development of rheumatic pain. In addition, the latter is also associated with impaired signaling in the nervous system and with psychological problems in patients.At the present stage, pain treatment includes non-pharmacological interventions, as well as the use of certain pharmacological agents, in particular opioids and narcotic drugs. However, despite significant successes in the design of drugs that relieve pain, at present, a significant proportion of patients with RDs still experience pain after therapy. When designing novel drugs for the treatment of pain, it is necessary to take into account the molecular mechanisms of its development in RDs. This review considers the features of the manifestations of pain, its molecular markers and mechanisms at different stages of the disease in patients with the two most common RDs, such as rheumatoid arthritis and osteoarthritis.
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Troshina, Ekaterina A., Maria A. Terekhova, and Ravida R. Akhmatova. "Immunological aspects of papillary thyroid cancer. What's new?" Clinical and experimental thyroidology 16, no. 4 (June 15, 2021): 14–18. http://dx.doi.org/10.14341/ket12695.
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Studying of the common links of pathogenesis of endocrine, autoimmune and oncological diseases is the area of interest of researchers from all countries of the world. Comprehension of artificially created mutual influences of molecular-genetic, immune factors that underlie the development and progression of endocrine tumors, primarily thyroid cancer, is important for creation and application of innovative treatment methods in oncoendocrinology.Today, the question of considering autoimmune diseases as a potential cause of oncological processes or on the contrary to consider them as protective conditions in some types of malignant tumors, remains controversial.In particular, autoimmune thyropathies and papillary thyroid cancer is an interesting model for studying these complex relationships. . The purpose of this article is to discuss accumulated experience, review the literature devoted to the study of immunological aspects in the pathogenesis of papillary thyroid cancer, reconsider obtained material and form a conclusion.
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Clemente, Nausicaa, Davide Raineri, Giuseppe Cappellano, Elena Boggio, Francesco Favero, Maria Felicia Soluri, Chiara Dianzani, Cristoforo Comi, Umberto Dianzani, and Annalisa Chiocchetti. "Osteopontin Bridging Innate and Adaptive Immunity in Autoimmune Diseases." Journal of Immunology Research 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/7675437.
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Osteopontin (OPN) regulates the immune response at multiple levels. Physiologically, it regulates the host response to infections by driving T helper (Th) polarization and acting on both innate and adaptive immunity; pathologically, it contributes to the development of immune-mediated and inflammatory diseases. In some cases, the mechanisms of these effects have been described, but many aspects of the OPN function remain elusive. This is in part ascribable to the fact that OPN is a complex molecule with several posttranslational modifications and it may act as either an immobilized protein of the extracellular matrix or a soluble cytokine or an intracytoplasmic molecule by binding to a wide variety of molecules including crystals of calcium phosphate, several cell surface receptors, and intracytoplasmic molecules. This review describes the OPN structure, isoforms, and functions and its role in regulating the crosstalk between innate and adaptive immunity in autoimmune diseases.
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Tenti, Sara, Pierpaolo Correale, Sara Cheleschi, Antonella Fioravanti, and Luigi Pirtoli. "Aromatase Inhibitors—Induced Musculoskeletal Disorders: Current Knowledge on Clinical and Molecular Aspects." International Journal of Molecular Sciences 21, no. 16 (August 6, 2020): 5625. http://dx.doi.org/10.3390/ijms21165625.
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Aromatase inhibitors (AIs) have radically changed the prognosis of hormone receptor positive breast cancer (BC) in post-menopausal women, and are a mainstay of the adjuvant therapy for BC after surgery in place of, or following, Tamoxifen. However, AIs aren’t side effect-free; frequent adverse events involve the musculoskeletal system, in the form of bone loss, AI-associated arthralgia (AIA) syndrome and autoimmune rheumatic diseases. In this narrative review, we reported the main clinical features of these three detrimental conditions, their influence on therapy adherence, the possible underlying molecular mechanisms and the available pharmacological and non-pharmacological treatments. The best-known form is the AIs-induced osteoporosis, whose molecular pathway and therapeutic possibilities were extensively investigated in the last decade. AIA syndrome is a high prevalent joint pain disorder which often determines a premature discontinuation of the therapy. Several points still need to be clarified, as a universally accepted diagnostic definition, the pathogenetic mechanisms and satisfactory management strategies. The association of AIs therapy with autoimmune diseases is of the utmost interest. The related literature has been recently expanded, but many issues remain to be explored, the first being the molecular mechanisms.
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Murashkin, Nikolay N., Alena A. Savelova, Roman A. Ivanov, Eduard T. Ambarchian, Alexander I. Materikin, Roman V. Epishev, and Leonid A. Opryatin. "Etiopathogenetic Similarities of Combined Forms of Localized Scleroderma and Vitiligo." Current Pediatrics 19, no. 6 (December 27, 2020): 452–59. http://dx.doi.org/10.15690/vsp.v19i6.2147.
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Vitiligo is a common skin disease characterized by idiopathic progressive skin hypomelanosis. Vitiligo is associated with several comorbid autoimmune diseases such as localized scleroderma. This article demonstrates the general development mechanism of these pathologies, as well as the key aspect of cross-effect between autoimmune diseases on the molecular level. Recently, dermatologists have noted the increasing number of patients suffering from combined pathologies. Such patients (in pediatrics) have torpid course of disease and no pathognomonic symptoms. That exaggerates the diagnostics and adequate therapy prescription. This leads to increased awareness among physicians of different specialties on possible combinations, clinical presentation and pathogenesis aspects of such conditions.
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Zakharova, M. Yu, T. A. Belyanina, A. V. Sokolov, I. S. Kiselev, and A. E. Mamedov. "The Contribution of Major Histocompatibility Complex Class II Genes to an Association with Autoimmune Diseases." Acta Naturae 11, no. 4 (December 15, 2019): 4–12. http://dx.doi.org/10.32607/20758251-2019-11-4-4-12.
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Genetic studies of patients with autoimmune diseases have shown that one of the most important roles in the developing of these diseases is played by a cluster of genes of the major histocompatibility complex (MHC), as compared with other genome areas. Information on the specific contribution of MHC alleles, mostly MHC class II ones, to the genetic predisposition to autoimmune diseases is crucial for understanding their pathogenesis. This review dwells on the most relevant aspects of this problem: namely, the correlation between carriage of certain MHC II alleles and an increased (positively associated allele) or reduced (negatively associated allele) probability of developing the most common autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, autoimmune thyroiditis, etc. The most universal haplotypes, DR3-DQ2 and DR4-DQ8, are positively associated with many of these diseases, while the universal allele HLA-DRB1*0701 is protective.
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PAPADOGIANNAKIS (E. Ι. ΠΑΠΑΔΟΓΙΑΝΝΑΚΗΣ), E. I. "Contemporary aspects on the immunopathogenesis of autoimmune diseases of the epidermal basement membrane in the dog." Journal of the Hellenic Veterinary Medical Society 56, no. 1 (November 29, 2017): 27. http://dx.doi.org/10.12681/jhvms.15066.
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Autoimmune diseases of the epidermal basement membrane are the result of the immune system self-activation against specific antigens of its essential structural elements. This group of skin diseases is characterized by the destruction of connecting bonds between the membrane zone and dermis, which eventually leads to the dermoepidermal separation and the formation of subepidermal vesicles and bullae. In this article, the immunopathogenesis and the clinical, histopathological and immunohistochemical features of each of these skin diseases are briefly reviewed. The autoimmune diseases of the canine epidermal basement membrane have been recently classified as bullous pemphigoid, mucous membrane pemphigoid, linear IgA dermatosis, epidermolysis bullosa acquisita and bullous systemic lupus erythematosus. Recent advances in immunopathological and molecular techniques have markedly facilitated the understanding of their pathogenesis, thus giving the opportunity for the development of new therapeutic strategies that may improve or eliminate the clinical signs.
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Makhneva, Nataliya V., Yu S. Butov, and V. Yu Vasenova. "THE MOLECULAR BIOLOGICAL AND IMMUNE PATHOLOGIC CHARACTERISTICS UNDER AUTO-IMMUNE DISEASES OF SKIN." Medical Journal of the Russian Federation 23, no. 5 (October 15, 2017): 258–62. http://dx.doi.org/10.18821/0869-2106-2017-23-5-258-262.
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The skin and mucous membranes are the min barrier organs providing systemic defense from environmental effects. They actively participate in deliverance of organism from antigens of various origin due to availability of one's own elements of immune system. The failure in chain of immune defense causes deceleration of process of elimination of antigen damaging structure of one's own tissue. The article presents mechanism of elimination of immune complexes and examples of therapeutic procedures accelerating and normalizing this process. The maintenance and recovery of excretory function of skin ensure positive dynamics of clinical manifestations of various diseases, including ones of autoimmune genesis. In case of fixation of immunoglobulins in tissues, skin acts as a target-organ. At that, detected specific antibodies are diagnostic markers for a wide circle of autoimmune dermatoses. Furthermore, immunopathologic processes occurring in skin are associated with disorders of synthesis of various molecular compounds of its tissue structures. This is testified by the results of immune morphologic picture of expression of a number of molecules of adhesion, protein components of desmosomal apparatus and basal membrane of epidermis, antigens of HLA-system. Therefore, skin is a complex organized structure capable to actively participate in development of inflammatory and autoimmune reactions. The analysis of these reactions at molecular biological level permits to evaluate intensity of occurring processes, to implement testing of efficacy of applied curative activities and in a number of cases to serve as an additional diagnostic marker. Undoubtedly, implementation of molecular biological methods as a tool of cognition favors continuous broadening of information about a number of aspects of pathogenesis of skin diseases and brings to development of new methods of their treatment at the molecular genetic level.
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Al-Dhahab, Hisham, Julia McNabb-Baltar, Said Al-Busafi, and Alan N. Barkun. "Immunoglobulin G4-Related Pancreatic and Biliary Diseases." Canadian Journal of Gastroenterology 27, no. 9 (2013): 523–30. http://dx.doi.org/10.1155/2013/180461.
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BACKGROUND: Autoimmune pancreatitis and autoimmune cholangitis are new clinical entities that are now recognized as the pancreaticobiliary manifestations of immunoglobulin (Ig) G4-related disease.OBJECTIVE: To summarize important clinical aspects of IgG4-related pancreatic and biliary diseases, and to review the role of IgG4 in the diagnosis of autoimmune pancreatitis (AIP) and autoimmune cholangitis (AIC).METHODS: A narrative review was performed using the PubMed database and the following keywords: “IgG4”, “IgG4 related disease”, “autoimmune pancreatitis”, “sclerosing cholangitis” and “autoimmune cholangitis”. A total of 955 articles were retrieved; of these, 381 contained relevant data regarding the IgG4 molecule, pathogenesis of IgG-related diseases, and diagnosis, management and long-term follow-up for patients with AIP and AIC. Of these 381 articles, 66 of the most pertinent were selected.RESULTS: The selected studies demonstrated the increasing clinical importance of both AIP and AIC, which can mimic pancreatic cancer and cholangiocarcinoma, respectively. IgG4 titration in tissue or blood cannot be used alone to diagnose all IgG4-related diseases; however, it is often a useful adjunct to clinical, radiological and histological features. AIP and AIC respond to steroids; however, relapse is common and long-term maintenance treatment often required.CONCLUSIONS: A review of the diagnosis and management of both AIC and AIP is timely and pertinent to clinical practice because the amount of information regarding these conditions has increased substantially in the past few years, resulting in significant impact on the clinical management of affected patients.
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Shi, Juan, Shuhong Chi, Jing Xue, Jiali Yang, Feng Li, and Xiaoming Liu. "Emerging Role and Therapeutic Implication of Wnt Signaling Pathways in Autoimmune Diseases." Journal of Immunology Research 2016 (2016): 1–18. http://dx.doi.org/10.1155/2016/9392132.
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The Wnt signaling pathway plays a key role in many biological aspects, such as cellular proliferation, tissue regeneration, embryonic development, and other systemic effects. Under a physiological condition, it is tightly controlled at different layers and arrays, and a dysregulated activation of this signaling has been implicated into the pathogenesis of various human disorders, including autoimmune diseases. Despite the fact that therapeutic interventions are available for ameliorating disease manifestations, there is no curative therapy currently available for autoimmune disorders. Increasing lines of evidence have suggested a crucial role of Wnt signaling during the pathogenesis of many autoimmune diseases; in addition, some of microRNAs (miRNAs), a class of small, noncoding RNA molecules capable of transcriptionally regulating gene expression, have also recently been demonstrated to possess both physiological and pathological roles in autoimmune diseases by regulating the Wnt signaling pathway. This review summarizes currently our understanding of the pathogenic roles of Wnt signaling in several major autoimmune disorders and miRNAs, those targeting Wnt signaling in autoimmune diseases, with a focus on the implication of the Wnt signaling as potential biomarkers and therapeutic targets in immune diseases, as well as miRNA-mediated regulation of Wnt signaling activation in the development of autoimmune diseases.
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Al Hadra, Bushra N. "Some of the Immunogenetics Aspects of Aging." Journal of Biomedical and Clinical Research 14, no. 1 (June 1, 2021): 16–30. http://dx.doi.org/10.2478/jbcr-2021-0003.
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Summary The human life span could be influenced by the combined effect of environment, lifestyle, and genetic factors. Twin and family studies suggest that our genes control up to 25% of the lifespan. The aging immune system undergoes age-associated changes at multiple levels, resulting in a gradual loss of its ability to protect the organism against infections, low vaccine responses, and an increased probability of developing autoimmune diseases and malignancies. The highly polymorphic HLA complex is one of the major gene candidates associated with aging due to its crucial role in developing adaptive immunity and protecting the organism. Most of the data available have so far demonstrated a positive association with healthy aging for HLA alleles/haplotypes as protective against malignancies, autoimmune diseases, and conferring better control and response to infections. One of aging’s main manifestations is the chronic, low-grade inflammatory state observed in older people, caused by an imbalance between pro- and anti-inflammatory cytokines. In general, it is has been agreed that longevity is related to anti-inflammatory genotype profiles. With advanced age, changes also occur in the B cell repertoire, which significantly affects the humoral immunity and leads to inadequate responses to infections and vaccines in the elderly. New genetic biomarkers associated with aging are being explored and discovered, contributing to a better understanding of the molecular processes underlying the immune dysfunction related to aging and developing strategies for rejuvenating the immune system based on immune-risk phenotypes.
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Drutskaya, M. S., E. O. Gubernatorova, E. A. Gorshkova, K. S. N. Athertkhany, M. A. Nosenko, V. S. Gogoleva, O. A. Namakanova, R. V. Zvartsev, A. A. Kruglov, and S. A. Nedospasov. "Cytokines, reverse genetics and anti-cytokine therapy." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 38–48. http://dx.doi.org/10.20538/1682-0363-2019-1-38-48.
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Cytokines comprise the molecular language of communication between the cells, which is needed to maintain the homeostatic functions of the body (including the immune system) and mediate various diseases. Many aspects of inflammation, autoimmune diseases and neoplasia are associated with cytokine signaling through specific receptors. The establishment of new physiological functions of “old” cytokines and understanding the molecular and cellular mechanisms of their involvement in disease pathogenesis, as well as the search for new therapeutic targets and development of innovative approaches to anti-cytokine therapy, present a fundamental problem. When assessing the tremendous success of anti-cytokine therapy in treatment of certain autoimmune diseases, we should not forget that (a) this treatment does not eliminate the causes of the disease:autoreactive T-cell clones; and that (b) less than half of the patients respond to this therapy; and that (c) anti-cytokine therapy has serious side effects.
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Lerner, Aaron, and Carina Benzvi. "“Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration." Cells 10, no. 4 (March 30, 2021): 756. http://dx.doi.org/10.3390/cells10040756.
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Wheat is a most favored staple food worldwide and its major protein is gluten. It is involved in several gluten dependent diseases and lately was suggested to play a role in non-celiac autoimmune diseases. Its involvement in neurodegenerative conditions was recently suggested but no cause-and-effect relationship were established. The present narrative review expands on various aspects of the gluten-gut-brain axes events, mechanisms and pathways that connect wheat and gluten consumption to neurodegenerative disease. Gluten induced dysbiosis, increased intestinal permeabillity, enteric and systemic side effects, cross-reactive antibodies, and the sequence of homologies between brain antigens and gluten are highlighted. This combination may suggest molecular mimicry, alluding to some autoimmune aspects between gluten and neurodegenerative disease. The proverb of Hippocrates coined in 400 BC, “let food be thy medicine,” is critically discussed in the frame of gluten and potential neurodegeneration evolvement.
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Alam, Jehan, Yong Chul Kim, and Youngnim Choi. "Potential Role of Bacterial Infection in Autoimmune Diseases: A New Aspect of Molecular Mimicry." Immune Network 14, no. 1 (2014): 7. http://dx.doi.org/10.4110/in.2014.14.1.7.
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El Hiani, Yassine, Emmanuel Eroume-A. Egom, and Xian-Ping Dong. "mTOR signalling: jack-of-all-trades." Biochemistry and Cell Biology 97, no. 1 (February 2019): 58–67. http://dx.doi.org/10.1139/bcb-2018-0004.
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The mechanistic target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase that senses and integrates environmental information into cellular regulation and homeostasis. Accumulating evidence has suggested a master role of mTOR signalling in many fundamental aspects of cell biology and organismal development. mTOR deregulation is implicated in a broad range of pathological conditions, including diabetes, cancer, neurodegenerative diseases, myopathies, inflammatory, infectious, and autoimmune conditions. Here, we review recent advances in our knowledge of mTOR signalling in mammalian physiology. We also discuss the impact of mTOR alteration in human diseases and how targeting mTOR function can treat human diseases.
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Hertelendy, Johannes, Georg Reumuth, David Simons, Christian Stoppe, Bong-Sung Kim, Jan-Philipp Stromps, Paul C. Fuchs, Jurgen Bernhagen, Norbert Pallua, and Gerrit Grieb. "Macrophage Migration Inhibitory Factor - A Favorable Marker in Inflammatory Diseases?" Current Medicinal Chemistry 25, no. 5 (February 13, 2018): 601–5. http://dx.doi.org/10.2174/0929867324666170714114200.
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Background: Macrophage migration inhibitory factor (MIF) was firstly described in the 1960s as a pleiotropic cytokine affecting a variety of immune cells. Different physiological functions mainly involving inflammatory reactions such as chemokine-like function and regulating systemic stress responses have been reported. Objective: In several clinical studies the use of MIF as a biomarker has been investigated promising support for diseases with an inflammatory aspect such as sepsis, systemic infections and autoimmune diseases. This article in detail reviews clinical data and evaluates the function as biomarker focusing on inflammatory and autoimmune diseases. Conclusion: Recent studies suggest MIF to be a marker for different inflammatory diseases and might serve as therapeutic target in the future.
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Wajda, Anna, Joanna Łapczuk-Romańska, and Agnieszka Paradowska-Gorycka. "Epigenetic Regulations of AhR in the Aspect of Immunomodulation." International Journal of Molecular Sciences 21, no. 17 (September 3, 2020): 6404. http://dx.doi.org/10.3390/ijms21176404.
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Environmental factors contribute to autoimmune disease manifestation, and as regarded today, AhR has become an important factor in studies of immunomodulation. Besides immunological aspects, AhR also plays a role in pharmacological, toxicological and many other physiological processes such as adaptive metabolism. In recent years, epigenetic mechanisms have provided new insight into gene regulation and reveal a new contribution to autoimmune disease pathogenesis. DNA methylation, histone modifications, chromatin alterations, microRNA and consequently non-genetic changes in phenotypes connect with environmental factors. Increasing data reveals AhR cross-roads with the most significant in immunology pathways. Although study on epigenetic modulations in autoimmune diseases is still not well understood, therefore future research will help us understand their pathophysiology and help to find new therapeutic strategies. Present literature review sheds the light on the common ground between remodeling chromatin compounds and autoimmune antibodies used in diagnostics. In the proposed review we summarize recent findings that describe epigenetic factors which regulate AhR activity and impact diverse immunological responses and pathological changes.
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Castro-Manrreza, Marta E., and Juan J. Montesinos. "Immunoregulation by Mesenchymal Stem Cells: Biological Aspects and Clinical Applications." Journal of Immunology Research 2015 (2015): 1–20. http://dx.doi.org/10.1155/2015/394917.
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Mesenchymal stem cells (MSCs) are multipotent cells capable of differentiation into mesenchymal lineages and that can be isolated from various tissues and easily cultivatedin vitro. Currently, MSCs are of considerable interest because of the biological characteristics that confer high potential applicability in the clinical treatment of many diseases. Specifically, because of their high immunoregulatory capacity, MSCs are used as tools in cellular therapies for clinical protocols involving immune system alterations. In this review, we discuss the current knowledge about the capacity of MSCs for the immunoregulation of immunocompetent cells and emphasize the effects of MSCs on T cells, principal effectors of the immune response, and the immunosuppressive effects mediated by the secretion of soluble factors and membrane molecules. We also describe the mechanisms of MSC immunoregulatory modulation and the participation of MSCs as immune response regulators in several autoimmune diseases, and we emphasize the clinical application in graft versus host disease (GVHD).
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Kak, Gunjan, Mohsin Raza, and Brijendra K. Tiwari. "Interferon-gamma (IFN-γ): Exploring its implications in infectious diseases." Biomolecular Concepts 9, no. 1 (May 30, 2018): 64–79. http://dx.doi.org/10.1515/bmc-2018-0007.
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AbstractA key player in driving cellular immunity, IFN-γ is capable of orchestrating numerous protective functions to heighten immune responses in infections and cancers. It can exhibit its immunomodulatory effects by enhancing antigen processing and presentation, increasing leukocyte trafficking, inducing an anti-viral state, boosting the anti-microbial functions and affecting cellular proliferation and apoptosis. A complex interplay between immune cell activity and IFN-γ through coordinated integration of signals from other pathways involving cytokines and Pattern Recognition Receptors (PRRs) such as Interleukin (IL)-4, TNF-α, Lipopolysaccharide (LPS), Type-I Interferons (IFNS) etc. leads to initiation of a cascade of pro-inflammatory responses. Microarray data has unraveled numerous genes whose transcriptional regulation is influenced by IFN-γ. Consequently, IFN-γ stimulated cells display altered expression of many such target genes which mediate its downstream effector functions. The importance of IFN-γ is further reinforced by the fact that mice possessing disruptions in the IFN-γ gene or its receptor develop extreme susceptibility to infectious diseases and rapidly succumb to them. In this review, we attempt to elucidate the biological functions and physiological importance of this versatile cytokine. The functional implications of its biological activity in several infectious diseases and autoimmune pathologies are also discussed. As a counter strategy, many virulent pathogenic species have devised ways to thwart IFN-γ endowed immune-protection. Thus, IFN-γ mediated host-pathogen interactions are critical for our understanding of disease mechanisms and these aspects also manifest enormous therapeutic importance for the annulment of various infections and autoimmune conditions.
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Zhang, Suisheng, and Frank Grosse. "Multiple Functions of Nuclear DNA Helicase II (RNA Helicase A) in Nucleic Acid Metabolism." Acta Biochimica et Biophysica Sinica 36, no. 3 (March 1, 2004): 177–83. http://dx.doi.org/10.1093/abbs/36.3.177.
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Abstract Nuclear DNA helicase II (NDH II), or RNA helicase A (RHA), was initially discovered in mammals by conventional protein purification methods. Molecular cloning identified apparent sequence homologies between NDH II and a Drosophila protein named maleless (MLE), the latter being essential for the Drosophila X-chromosome dosage compensation. Increasing amounts of evidence suggest that NDH II is involved in multiple aspects of cellular and viral DNA and RNA metabolism. Moreover the functions of NDH II may have potential clinical implications related to viral infection, autoimmune diseases, or even tumorigenesis.
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Albornoz, Nicolas, Hianara Bustamante, Andrea Soza, and Patricia Burgos. "Cellular Responses to Proteasome Inhibition: Molecular Mechanisms and Beyond." International Journal of Molecular Sciences 20, no. 14 (July 10, 2019): 3379. http://dx.doi.org/10.3390/ijms20143379.
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Proteasome inhibitors have been actively tested as potential anticancer drugs and in the treatment of inflammatory and autoimmune diseases. Unfortunately, cells adapt to survive in the presence of proteasome inhibitors activating a variety of cell responses that explain why these therapies have not fulfilled their expected results. In addition, all proteasome inhibitors tested and approved by the FDA have caused a variety of side effects in humans. Here, we describe the different types of proteasome complexes found within cells and the variety of regulators proteins that can modulate their activities, including those that are upregulated in the context of inflammatory processes. We also summarize the adaptive cellular responses activated during proteasome inhibition with special emphasis on the activation of the Autophagic-Lysosomal Pathway (ALP), proteaphagy, p62/SQSTM1 enriched-inclusion bodies, and proteasome biogenesis dependent on Nrf1 and Nrf2 transcription factors. Moreover, we discuss the role of IRE1 and PERK sensors in ALP activation during ER stress and the involvement of two deubiquitinases, Rpn11 and USP14, in these processes. Finally, we discuss the aspects that should be currently considered in the development of novel strategies that use proteasome activity as a therapeutic target for the treatment of human diseases.
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Cebeci, Filiz, Nahide Onsun, Ayşe Pekdemir, Ahmet R. Uras, and Kadir Kayataş. "Thyroid Autoimmunity and Behçet’s Disease: Is There a Significant Association?" Scientific World Journal 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/956837.
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Background. Behcet’s disease (BD) could be regarded as an autoimmune disease in many aspects. Autoimmune thyroid disease (ATD) is frequently accompanied by other various autoimmune diseases. Nevertheless, there is not still enough data showing the association between BD and ATD. In addition, no controlled study is present in the PubMed, which evaluates thyroidal autoimmunity using antithyroid peroxidase antibody in a large series of patients with BD.Methods. We aimed to investigate the frequency of ATD in patients with BD. The study included 124 patients with BD and 99 age- and sex-matched healthy volunteers.Results. Autoimmune thyroiditis was noted in 21 cases (16.9%) with BD. In the control group, 22 cases (22.22%) were diagnosed as autoimmune thyroiditis. There was no difference between the groups in respect to thyroid autoantibodies (). There were no statistically significant differences between baseline TSH levels of the BD patients and of the controls (). Statistically, the mean serum free T4 levels of the patients with BD were higher than those of the controls ().Conclusions. No association could be found between BD and ATD. Therefore, it is not of significance to investigate thyroid autoimmunity in BD.
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Ventriglia, Giuliana, Laura Nigi, Guido Sebastiani, and Francesco Dotta. "MicroRNAs: Novel Players in the Dialogue between Pancreatic Islets and Immune System in Autoimmune Diabetes." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/749734.
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MicroRNAs are small noncoding RNA molecules that regulate gene expression in all cell types. Therefore, these tiny noncoding RNA molecules are involved in a wide range of biological processes, exerting functional effects at cellular, tissue, and organ level. In pancreatic islets of Langerhans, including beta-cells, microRNAs are involved in cell differentiation as well as in insulin secretion, while in immune cells they have been shown to play pivotal roles in development, activation, and response to antigens. Indeed, it is not surprising that microRNA alterations can lead to the development of several diseases, including type 1 diabetes (T1D). Type 1 diabetes is the result of a selective autoimmune destruction of insulin-producing beta-cells, characterized by islet inflammation (insulitis), which leads to chronic hyperglycemia. Given the growing importance of microRNA in the pathophysiology of T1D, the aim of this review is to summarize the most recent data on the potential involvement of microRNAs in autoimmune diabetes. Specifically, we will focus on three different aspects: (i) microRNAs as regulators of immune homeostasis in autoimmune diabetes; (ii) microRNA expression in pancreatic islet inflammation; (iii) microRNAs as players in the dialogue between the immune system and pancreatic endocrine cells.
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D'Agosto, G., A. Latini, M. Carducci, A. Mastroianni, A. Vento, and P. Cordiali Fei. "Evaluation of Recombinant Antigen-Based Assays for Diagnosis of Bullous Autoimmune Diseases." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 762–65. http://dx.doi.org/10.1128/cdli.11.4.762-765.2004.
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ABSTRACT The diagnosis of autoimmune bullous diseases is based on clinical observation and on the presence of autoantibodies directed to molecules involved in the adhesion systems of the skin. Immunofluorescence assays are the currently accepted method for detection of autoantibodies; such assays depend greatly on the skill of operators and are difficult to standardize. Recombinant desmoglein-1 (Dsg1), Dsg3, and BP180 peptides, the main autoantigens in pemphigus or bullous pemphigoid, have been used to develop new quantitative enzyme immunoassays (EIA) for the detection of specific antibodies. The present study was undertaken to evaluate the sensitivity and specificity of these immunoassays and to determine the correlation between the results and the clinical aspects of diseases. Serum samples from patients with pemphigus vulgaris, pemphigus foliaceus, bullous pemphigoid, or mucous membrane pemphigoid, from healthy individuals, and from patients with unrelated autoimmune conditions were tested. Anti-desmoglein reactivity was detected in all the patients with pemphigus and in none of the controls. Patients with the more benign form of cutaneous disease had anti-Dsg1 antibodies, while patients with deeper cutaneous lesions or with mucosal involvement had anti-Dsg3 reactivity also, or exclusively. The BP180-based assay was positive for 66.6% of patients with bullous pemphigoid and for none of the patients with mucous membrane pemphigoid, and no reactivity was detected in the control sera. In conclusion, the anti-Dsg1 and anti-Dsg3 assays are useful in the diagnosis of pemphigus and provide information on the clinical phenotype of the disease. However, the sensitivity of EIA for detection of autoantibodies in bullous pemphigoid should be improved by the use of additional antigens or epitopes.
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Darlan, Dewi Masyithah, Muhammad Fakhrur Rozi, and Hemma Yulfi. "Overview of Immunological Responses and Immunomodulation Properties of Trichuris sp.: Prospects for Better Understanding Human Trichuriasis." Life 11, no. 3 (February 27, 2021): 188. http://dx.doi.org/10.3390/life11030188.
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Trichuris sp. infection has appeared as a pathological burden in the population, but the immunomodulation features could result in an opportunity to discover novel treatments for diseases with prominent inflammatory responses. Regarding the immunological aspects, the innate immune responses against Trichuris sp. are also responsible for determining subsequent immune responses, including the activation of innate lymphoid cell type 2 (ILC2s), and encouraging the immune cell polarization of the resistant host phenotype. Nevertheless, this parasite can establish a supportive niche for worm survival and finally avoid host immune interference. Trichuris sp. could skew antigen recognition and immune cell activation and proliferation through the generation of specific substances, called excretory/secretory (ESPs) and soluble products (SPs), which mainly mediate its immunomodulation properties. Through this review, we elaborate and discuss innate–adaptive immune responses and immunomodulation aspects, as well as the clinical implications for managing inflammatory-based diseases, such as inflammatory bowel diseases, allergic, sepsis, and other autoimmune diseases.
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Aparicio-Soto, Marina, Marina Sánchez-Hidalgo, and Catalina Alarcón-de-la-Lastra. "An update on diet and nutritional factors in systemic lupus erythematosus management." Nutrition Research Reviews 30, no. 1 (March 15, 2017): 118–37. http://dx.doi.org/10.1017/s0954422417000026.
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AbstractSystemic lupus erythematosus (SLE) is a chronic inflammatory and autoimmune disease characterised by multiple organ involvement and a large number of complications. SLE management remains complicated owing to the biological heterogeneity between patients and the lack of safe and specific targeted therapies. There is evidence that dietary factors can contribute to the geoepidemiology of autoimmune diseases such as SLE. Thus, diet therapy could be a promising approach in SLE owing to both its potential prophylactic effects, without the side effects of classical pharmacology, and its contribution to reducing co-morbidities and improving quality of life in patients with SLE. However, the question arises as to whether nutrients could ameliorate or exacerbate SLE and how they could modulate inflammation and immune function at a molecular level. The present review summarises preclinical and clinical experiences to provide the reader with an update of the positive and negative aspects of macro- and micronutrients and other nutritional factors, including dietary phenols, on SLE, focusing on the mechanisms of action involved.
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Ivanov, Dmitry O., Valentina V. Malinovskaya, Vladimir N. Timchenko, Tatyana A. Kaplina, and Jean-Claude Hakizimana. "Global and pediatric aspects of Zika virus infection." Pediatrician (St. Petersburg) 7, no. 1 (March 15, 2016): 129–34. http://dx.doi.org/10.17816/ped71129-134.
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This article presents the results of data analysis or references on etiology, epidemiology, pathogenesis, clinical features, therapy and prophylaxis of Zika virus infection. The article presents the results of the literature analysis of the data on the etiology, epidemiology, pathogenesis, clinical presentation, treatment and prevention of Zika virus infection. Currently Zika fever is common in tropical climates (Uganda, Brazil, Haiti, Colombia, Ecuador, El Salvador, Venezuela, Jamaica, Thailand, etc.). However, a large number of travelers and areolas mosquito habitat Αedes kind of make this a global problem. Acquired Zika virus infection usually occurs in mild and/or moderate forms. The development of severe forms occurs mainly in people with a weakened immune system or autoimmune diseases. Patients affected with Zika virus may develop neurological complications such as encephalitis, myelitis, optic neuritis, meningoencephalitis, Guillain-Barre syndrome. Transplacental and sexual transmissions contribute to an increase in the number of cases among children, including newborns. Zika congenital infection is characterized with brain damage, hearing and sight. Acquired Zika fever in children is accompanied by the presence of the following syndromes: subfebrile fever, mild intoxication, maculopapular rash with a landmark distribution, arthralgia, myalgia, photophobia and conjunctivitis, diarrhea rarely observed. In the laboratory diagnosis are used virological, molecular biological and serological methods. There are no specific prophylactic methods.To treat Zika virus infection, may be used recombinant human inteferona α2β and interferon inducers.
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Patiño-Trives, A. M., C. Perez-Sanchez, A. Ibañez-Costa, P. S. Laura, M. Luque-Tévar, I. Arias de la Rosa, M. C. Ábalos-Aguilera, et al. "OP0038 SPLICEOSOME ALTERATIONS IN LEUCOCYTES FROM APS, SLE AND SLE+APS PATIENTS ARE CLOSELY RELATED TO THEIR MAIN CLINICAL FEATURES." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 20.2–20. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2485.
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Background:To date, although multiple molecular approaches have illustrated the various aspects of Primary Antiphospholipid Syndrome (APS), systemic lupus erythematosus (SLE) and antiphospholipid syndrome plus lupus (APS plus SLE), no study has so far fully characterized the potential role of posttranscriptional regulatory mechanisms such as the alternative splicing.Objectives:To identify shared and differential changes in the splicing machinery of immune cells from APS, SLE and APS plus SLE patients, and their involvement in the activity and clinical profile of these autoimmune disorders.Methods:Monocytes, lymphocytes and neutrophils from 80 patients (22 APS, 35 SLE and 23 APS plus SLE) and 50 healthy donors (HD) were purified by immunomagnetic selection. Then, selected elements of the splicing machinery were evaluated using a microfluidic qPCR array (Fluidigm). In parallel, extensive clinical/serological evaluation was performed, comprising disease activity, thrombosis and renal involvement, along with autoantibodies, acute phase reactants, complement and inflammatory molecules. Molecular clustering analyses and correlation/association studies were developed.Results:Patients with primary APS, SLE and APS plus SLE displayed significant and specific alterations in the splicing machinery components in comparison with HD, that were further specific for each leukocyte subset. Besides, these alterations were associated with distinctive clinical features.Hence, in APS, clustering analysis allowed to identify two sets of patients representing different molecular profile groups with respect to the expression levels of splicing machinery components. Principal component analyses confirmed a clear separation between patients. Clinically, cluster 1 characterized patients with higher thrombotic episodes and recurrences than cluster 2 and displayed a higher adjusted global APS score (aGAPSS). Accordingly, these patients showed higher levels of inflammatory mediators than cluster 2.Similarly, in patients with APS plus SLE, clustering analysis allowed to identify two sets of patients showing differential expression of splicing machinery components. Clinical and laboratory profiles showed that cluster 2 characterized patients that had suffered more thrombotic recurrences, most of them displaying an aGAPSS over 12 points and expressing higher levels of inflammatory mediators than cluster 1. The incidence of lupus nephropathy was similarly represented in both clusters.Lastly, in SLE patients, molecular clustering analysis identified two sets of patients showing distinctive clinical features. One cluster characterized most of the patients positive for anti-dsDNA antibodies, further suffering lupus nephropathy, and a high proportion of them also presenting atheroma plaques and high levels of inflammatory mediators.Correlation studies further demonstrated that several deranged splicing machinery components in immune cells (i.e. SF3B1tv1, PTBP1, PRP8 and RBM17) were linked to the autoimmune profile of the three autoimmune diseases, albeit in a specific way on each disorder. Accordingly, in vitro treatment of HD lymphocytes with aPL-IgG or anti-dsDNA-IgG changed the expression of spliceosome components also found altered in vivo in the three autoimmune diseases. Finally, the induced over/downregulated expression of selected spliceosome components in leukocytes modulated the expression of inflammatory cytokines, changed the procoagulant/adhesion activities of monocytes and regulated NETosis in neutrophils.Conclusion:1) The splicing machinery, profoundly altered in leukocytes from APS, APS plus SLE and SLE patients, is closely related to the activity of these diseases, their autoimmune and inflammatory profiles. 2) The analysis of the splicing machinery allows the segregation of APS, APS plus SLE and SLE, with specific components explaining the CV risk and renal involvement in these highly related autoimmune disorders.Acknowledgements:Funded by ISCIII, PI18/00837 and RIER RD16/0012/0015 co-funded with FEDERDisclosure of Interests:None declared
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Rusca, Nicole, and Silvia Monticelli. "MiR-146a in Immunity and Disease." Molecular Biology International 2011 (April 7, 2011): 1–7. http://dx.doi.org/10.4061/2011/437301.
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MicroRNAs (miRNAs) are regulatory molecules able to influence all aspects of the biology of a cell. They have been associated with diseases such as cancer, viral infections, and autoimmune diseases, and in recent years, they also emerged as important regulators of immune responses. MiR-146a in particular is rapidly gaining importance as a modulator of differentiation and function of cells of the innate as well as adaptive immunity. Given its importance in regulating key cellular functions, it is not surprising that miR-146a expression was also found dysregulated in different types of tumors. In this paper, we summarize recent progress in understanding the role of miR-146a in innate and adaptive immune responses, as well as in disease.
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Sabir, Fakhara, Muhammad Imran Asad, Maimoona Qindeel, Iqra Afzal, Muhammad Junaid Dar, Kifayat Ullah Shah, Alam Zeb, Gul Majid Khan, Naveed Ahmed, and Fakhar-ud Din. "Polymeric Nanogels as Versatile Nanoplatforms for Biomedical Applications." Journal of Nanomaterials 2019 (May 16, 2019): 1–16. http://dx.doi.org/10.1155/2019/1526186.
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Nanomaterials have found extensive biomedical applications in the past few years because of their small size, low molecular weight, larger surface area, enhanced biological, and chemical reactivity. Among these nanomaterials, nanogels (NGs) are promising drug delivery systems and are composed of cross-linked polymeric nanoparticles ranging from 100 to 200 nm. NGs represent an innovative zone of research with speedy developments taking place on a daily basis. An incredible amount of focus is placed on the fabrication of NGs with novel polymers to achieve better control over the drug release. This review article covers a number of aspects of NGs including their types, associated pros and cons, and methods of preparation along with technical and economical superiority and therapeutic efficacy over each other. The last part of review summarizes the applications of NGs in the drug delivery and treatment of various diseases including brain disease, cardiovascular diseases, oxidative stress, diabetes, cancer therapy, tissue engineering, gene therapy, inflammatory disorders, pain management, ophthalmic and autoimmune diseases, and their future challenges. NGs appear to be an outstanding nominee for drug delivery systems, and further study is required to explore their interactions at the cellular and molecular levels.
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Posadas, I., L. Romero-Castillo, N. El Brahmi, D. Manzanares, S. Mignani, J. P. Majoral, and V. Ceña. "Neutral high-generation phosphorus dendrimers inhibit macrophage-mediated inflammatory response in vitro and in vivo." Proceedings of the National Academy of Sciences 114, no. 37 (August 28, 2017): E7660—E7669. http://dx.doi.org/10.1073/pnas.1704858114.
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Inflammation is part of the physiological response of the organism to infectious diseases caused by organisms such as bacteria, viruses, fungi, or parasites. Innate immunity, mediated by mononuclear phagocytes, including monocytes and macrophages, is a first line of defense against infectious diseases and plays a key role triggering the delayed adaptive response that ensures an efficient defense against pathogens. Monocytes and macrophages stimulation by pathogen antigens results in activation of different signaling pathways leading to the release of proinflammatory cytokines. However, inflammation can also participate in the pathogenesis of several diseases, the autoimmune diseases that represent a relevant burden for human health. Dendrimers are branched, multivalent nanoparticles with a well-defined structure that have a high potential for biomedical applications. To explore new approaches to fight against the negative aspects of inflammation, we have used neutral high-generation phosphorus dendrimers bearing 48 (G3) or 96 (G4) bisphosphonate groups on their surface. These dendrimers show no toxicity and have good solubility and chemical stability in aqueous solutions. Here, we present data indicating that neutral phosphorus dendrimers show impressive antiinflammatory activities both in vitro and in vivo. In vitro, these dendrimers reduced the secretion of proinflammatory cytokines from mice and human monocyte-derived macrophages. In addition, these molecules present efficient antiinflammatory activity in vivo in a mouse model of subchronic inflammation. Taken together, these data suggest that neutral G3-G4 phosphorus dendrimers have strong potential applications in the therapy of inflammation and, likely, of autoimmune diseases.
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Markovic, Milica, Shimon Ben-Shabat, Aaron Aponick, Ellen M. Zimmermann, and Arik Dahan. "Lipids and Lipid-Processing Pathways in Drug Delivery and Therapeutics." International Journal of Molecular Sciences 21, no. 9 (May 4, 2020): 3248. http://dx.doi.org/10.3390/ijms21093248.
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The aim of this work is to analyze relevant endogenous lipid processing pathways, in the context of the impact that lipids have on drug absorption, their therapeutic use, and utilization in drug delivery. Lipids may serve as biomarkers of some diseases, but they can also provide endogenous therapeutic effects for certain pathological conditions. Current uses and possible clinical benefits of various lipids (fatty acids, steroids, triglycerides, and phospholipids) in cancer, infectious, inflammatory, and neurodegenerative diseases are presented. Lipids can also be conjugated to a drug molecule, accomplishing numerous potential benefits, one being the improved treatment effect, due to joined influence of the lipid carrier and the drug moiety. In addition, such conjugates have increased lipophilicity relative to the parent drug. This leads to improved drug pharmacokinetics and bioavailability, the ability to join endogenous lipid pathways and achieve drug targeting to the lymphatics, inflamed tissues in certain autoimmune diseases, or enable overcoming different barriers in the body. Altogether, novel mechanisms of the lipid role in diseases are constantly discovered, and new ways to exploit these mechanisms for the optimal drug design that would advance different drug delivery/therapy aspects are continuously emerging.
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Khammissa, R. A. G., R. Chandran, A. Masilana, J. Lemmer, and L. Feller. "Adverse Immunologically Mediated Oral Mucosal Reactions to Systemic Medication: Lichenoid Tissue Reaction/Interface Dermatitis-Stomatitis, Autoimmune Vesiculobullous Disease, and IgE-Dependent and Immune Complex Reactions." Journal of Immunology Research 2018 (June 10, 2018): 1–10. http://dx.doi.org/10.1155/2018/7645465.
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Drug-induced hypersensitivity immune reactions are exaggerated immunoinflammatory responses to allergenic components of the medications that occur in genetically susceptible subjects. The type of hypersensitivity immune response generated, whether antibody mediated or T cell mediated, or an immune complex reaction is determined by multiple factors, including the molecular characteristics of the allergen, the route of administration of the medication, the manner of presentation of the allergen by antigen-presenting cells to naïve T cells, the repertoire of the T cell receptors, and the cytokine profile within the microenvironment. This review deals with the clinical and histopathological aspects of adverse immunologically mediated oral mucosal reactions to systemic medication. We elaborate on diseases showing features of lichenoid tissue reaction/interface dermatitis-stomatitis, autoimmune vesiculobullous oral lesions, and immunoglobulin E- (IgE-) and immune complex-mediated oral reactions to drugs.
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Ferreira, Maria Angélica, Caroline Lacerda, and Leila Moreira. "PD31 Financial Impact Of Target Molecular Therapies In A Brazilian Hospital." International Journal of Technology Assessment in Health Care 34, S1 (2018): 140–41. http://dx.doi.org/10.1017/s0266462318003045.
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Introduction:The therapy using molecular-targeted (MTT) and monoclonal antibodies (MA) are examples of new therapeutic technologies in search of greater clinical effectiveness and reduction of adverse effects in the fight against frequent diseases. Generally, new technologies have a high cost impact on the health system. The objective of this study was to evaluate the financial impact generated by the use of MTT and MA therapies in the teaching Hospital de Clínicas, Porto Alegre, Brazil.Methods:The first 60 higher monetary spending drug items of the last 12 months were analyzed. From them, drugs which fit in the categories under study, and have been regularly used, were identified. The monthly expenditures with each item were tabulated and compared with the total expenditures on drugs, in order to calculate the budgetary impact. The major groups of diseases treated with each agent were analyzed.Results:Two MTT agents (gefitinib and infliximab) and three MAs (rituximab, basiliximab and abciximab) were identified. The highest expenditure items, respectively, per year, were the oncological medicines rituximab (USD127,890) and gefitinib (USD96,923), followed by the immunosuppressive basiliximab (USD88,998) and the immunomodulatory infliximab (USD68,642), and the platelet aggregation inhibitor abciximab (USD47,886). These values corresponding to, respectively, 1.1 percent, 0.8 percent, 0.8 percent, 0.6 percent and 0.4 percent of total drug expenditure per year (USD11,866,124). Trastuzumab, bortezomib and imatinib were often used, but directly supplied by the public system, in a way that didn't impact the hospital budgetary management.Conclusions:MTT and MA have an important impact on health budgets, and are mainly used to treat some types of cancer, cardiovascular disease and autoimmune disorders. These aspects should be considered in the management of drugs in hospitals of high complexity.
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Magdy Beshbishy, Amany, Saad Alghamdi, ThankGod E. Onyiche, Muhammad Zahoor, Nallely Rivero-Perez, Adrian Zaragoza-Bastida, Mohamed A. Ghorab, et al. "Biogenesis, Biologic Function and Clinical Potential of Exosomes in Different Diseases." Applied Sciences 10, no. 13 (June 27, 2020): 4428. http://dx.doi.org/10.3390/app10134428.
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Exosomes are extracellular vesicles (EVs) belonging to the nanovesicles family that function as signaling molecules between cells. After their first description in the late 1960s, interest in their potential as a research target has steadily increased. They are small secreted organelles with a single membrane that are well enriched in lipids, proteins, nucleic acids, and glycoconjugates. Exosomes take part in a larger communication network in which cells communicate between one another by DNA shuttling, proteins, RNA, and membrane-bound factors. The machinery of protein quality control occurs through the process termed “exosome biogenesis”. Furthermore, the pathway involved in intercellular movement of vesicles is vital in various aspects of human health and diseases. Due to their inherent properties, exosomes are currently being developed as potential therapeutic agents in a wide range of diseases including infectious and non-infectious diseases. Exosomes and other EVs sourced from Mesenchymal stem cells (MSCs) have been shown in different studies to possess therapeutic effects in diverse disease models either in vivo or in vitro. Some mechanisms and/or pathways that MSC-derived exosomes use to illustrate their therapeutic effect against some diseases have also been summarized. This review aims to highlight the recent findings and potential therapeutic application of exosomes in different diseases such as autoimmune, cardiovascular, obesity, neural, soft tissues, bone, and cartilage.
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Vojvodic, Aleksandra, Zorica Peric-Hajzler, Dusica Matovic, Petar Vojvodic, Tatjana Vlaskovic-Jovicevic, Goran Sijan, Sanja Dimitrijevic, et al. "Gut Microbiota and the Alteration of Immune Balance in Skin Diseases: From Nutraceuticals to Fecal Transplantation." Open Access Macedonian Journal of Medical Sciences 7, no. 18 (September 12, 2019): 3034–38. http://dx.doi.org/10.3889/oamjms.2019.827.
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T
The P.N.E.I. (Psycho-Neuro-Endocrine-Immunology) approach is represented by the interdisciplinary concept of bidirectional cross-talk between the psycho-neuro-endocrine and immune systems, which can influence the immune response. The well-known Gut-Brain Axis and the Gut-Skin Axis can be merged in a bigger network- the Gut-Brain-Skin Axis, with complex regulation by cytokines, neuro-peptides, neuro-hormones and another messenger (signalling) molecules and maybe the most important modulator of the Gut-Brain-Skin Axis/ the gut microbiota. The role of gut bacterial homeostasis is very important, and the homeostatic imbalance of the immune response may be a relevant etiologic/pathophysiologic factor for extra-intestinal and intestinal inflammatory, allergic and autoimmune diseases. The Low Dose Cytokines Medicine (LDM) is an innovative therapeutic approach. It is based on the most advanced knowledge in molecular biology and low dose pharmacology with the primary outcome. The SKA (Sequential Kinetic Activation) technology, codified and standardised by GUNA S.p.a. -Italy- makes the low doses of signalling molecules able to be active even below the minimum dose classically considered as effective and the significative efficacy of orally administered low-dose signalling molecules is the most representative aspect of LDM. The Physiologic Nutraceuticals and the Low Dose Medicine are two of the most promising approaches for the treatment of skin diseases based on the rebalance of the immune response and the recovery of gut dysbiosis.
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Kothavade, Pankaj S., Dnyaneshwar M. Nagmoti, Vipin D. Bulani, and Archana R. Juvekar. "Arzanol, a Potent mPGES-1 Inhibitor: Novel Anti-Inflammatory Agent." Scientific World Journal 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/986429.
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Arzanol is a novel phloroglucinolα-pyrone, isolated from a Mediterranean plantHelichrysum italicum(Roth) Don ssp.microphyllumwhich belongs to the family Asteraceae. Arzanol has been reported to possess a variety of pharmacological activities. However, anti-inflammatory, anti-HIV, and antioxidant activities have been studied in some detail. Arzanol has been reported to inhibit inflammatory transcription factor NFκB activation, HIV replication in T cells, releases of IL-1β, IL-6, IL-8, and TNF-α, and biosynthesis of PGE2by potentially inhibiting mPGES-1 enzyme. Diversity of mechanisms of actions of arzanol may be useful in treatment of disease involving these inflammatory mediators such as autoimmune diseases and cancer. This review presents comprehensive information on the chemistry, structure-activity relationship, and pharmacological activities of arzanol. In addition this review discusses recent developments and the scope for future research in these aspects.
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Di Battista, Valeria, Maria Teresa Bochicchio, Giulio Giordano, Mariasanta Napolitano, and Alessandro Lucchesi. "Genetics and Pathogenetic Role of Inflammasomes in Philadelphia Negative Chronic Myeloproliferative Neoplasms: A Narrative Review." International Journal of Molecular Sciences 22, no. 2 (January 8, 2021): 561. http://dx.doi.org/10.3390/ijms22020561.
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The last decade has been very important for the quantity of preclinical information obtained regarding chronic myeloproliferative neoplasms (MPNs) and the following will be dedicated to the translational implications of the new biological acquisitions. The overcoming of the mechanistic model of clonal evolution and the entry of chronic inflammation and dysimmunity into the new model are the elements on which to base a part of future therapeutic strategies. The innate immune system plays a major role in this context. Protagonists of the initiation and regulation of many pathological aspects, from cytokine storms to fibrosis, the NLRP3 and AIM2 inflammasomes guide and condition the natural history of the disease. For this reason, MPNs share many biological and clinical aspects with non-neoplastic diseases, such as autoimmune disorders. Finally, cardiovascular risk and disturbances in iron metabolism and myelopoiesis are also closely linked to the role of inflammasomes. Although targeted therapies are already being tested, an increase in knowledge on the subject is desirable and potentially translates into better care for patients with MPNs.
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Di Battista, Valeria, Maria Teresa Bochicchio, Giulio Giordano, Mariasanta Napolitano, and Alessandro Lucchesi. "Genetics and Pathogenetic Role of Inflammasomes in Philadelphia Negative Chronic Myeloproliferative Neoplasms: A Narrative Review." International Journal of Molecular Sciences 22, no. 2 (January 8, 2021): 561. http://dx.doi.org/10.3390/ijms22020561.
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The last decade has been very important for the quantity of preclinical information obtained regarding chronic myeloproliferative neoplasms (MPNs) and the following will be dedicated to the translational implications of the new biological acquisitions. The overcoming of the mechanistic model of clonal evolution and the entry of chronic inflammation and dysimmunity into the new model are the elements on which to base a part of future therapeutic strategies. The innate immune system plays a major role in this context. Protagonists of the initiation and regulation of many pathological aspects, from cytokine storms to fibrosis, the NLRP3 and AIM2 inflammasomes guide and condition the natural history of the disease. For this reason, MPNs share many biological and clinical aspects with non-neoplastic diseases, such as autoimmune disorders. Finally, cardiovascular risk and disturbances in iron metabolism and myelopoiesis are also closely linked to the role of inflammasomes. Although targeted therapies are already being tested, an increase in knowledge on the subject is desirable and potentially translates into better care for patients with MPNs.
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Sennikov, S. V., A. A. Alshevskaya, J. V. Zhukova, I. A. Belomestnova, A. V. Karaulov, and J. A. Lopatnikova. "EXPRESSION DENSITY OF RECEPTORS TO IMMUNOREGULATORY MEDIATORS AS A MODULATING COMPONENT OF BIOLOGICAL EFFECTS OF MEDIATORS ON CELL. PART 1." Medical Immunology (Russia) 21, no. 2 (May 21, 2019): 209–20. http://dx.doi.org/10.15789/1563-0625-2019-2-209-220.
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The present review article summarizes the latest world scientific data on the role of receptors for immune mediators in regulating biological effects on the cells. For the main classes of immune regulators (interleukins, interferons, growth factors and tumor necrosis factors), the variants are presented for participation of receptors as components of cytokine/cell interaction, as proven by in vitro and in vivo studies. Ability of the receptors expression to modify characteristics and type of these interactions is shown. The data on participation of receptors for regulatory molecules in development of immune-mediated diseases of various genesis have been analyzed. It was demonstrated that the changes in the receptor expression are of great importance when evaluating functional response of the cells to the mediators and in development of pathological conditions. Current studies confirmed the data suggesting effects of receptor density upon the processes of proliferation and apoptosis, as well as metabolic processes that trigger development of autoimmune, oncological and dystrophic diseases. For all the considered classes of regulatory molecules, the change in the density of receptor expression is one of the key aspects in regulating functional activity of the cells. Thus, studying expression levels of receptors on the cell membrane is important in understanding pathogenesis, whereas changing expression level may be considered as a therapeutic target in the treatment of various diseases.
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Sennikov, S. V., A. A. Alshevskaya, Yu V. Zhukova, I. A. Belomestnova, A. V. Karaulov, and Yu A. Lopatnikova. "EXPRESSION DENSITY OF RECEPTORS FOR IMMUNOREGULATORY MEDIATORS AS A MODULATORY COMPONENT OF BIOLOGICAL EFFECTS OF MEDIATORS UPON CELLS (PART 2)." Medical Immunology (Russia) 21, no. 3 (July 13, 2019): 379–96. http://dx.doi.org/10.15789/1563-0625-2019-3-379-396.
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The present review article summarizes the latest world scientific data on the role of receptors for immune mediators in regulating biological effects on the cells. For the main classes of immune regulators (interleukins, interferons, growth factors and tumor necrosis factors), the variants are presented for participation of receptors as components of cytokine/cell interaction, as proven byin vitroandin vivostudies. Ability of the receptors expression to modify characteristics and type of these interactions is shown. The data on participation of receptors for regulatory molecules in development of immune-mediated diseases of various genesis have been analyzed. It was demonstrated that the changes in the receptor expression are of great importance when evaluating functional response of the cells to the mediators and in development of pathological conditions. Current studies confirmed the data suggesting effects of receptor density upon the processes of proliferation and apoptosis, as well as metabolic processes that trigger development of autoimmune, oncological and dystrophic diseases. For all the considered classes of regulatory molecules, the change in the density of receptor expression is one of the key aspects in regulating functional activity of the cells. Thus, studying expression levels of receptors on the cell membrane is important in understanding pathogenesis, whereas changing expression level may be considered as a therapeutic target in the treatment of various diseases.
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Vesperini, Doriane, Galia Montalvo, Bin Qu, and Franziska Lautenschläger. "Characterization of immune cell migration using microfabrication." Biophysical Reviews 13, no. 2 (February 11, 2021): 185–202. http://dx.doi.org/10.1007/s12551-021-00787-9.
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AbstractThe immune system provides our defense against pathogens and aberrant cells, including tumorigenic and infected cells. Motility is one of the fundamental characteristics that enable immune cells to find invading pathogens, control tissue damage, and eliminate primary developing tumors, even in the absence of external treatments. These processes are termed “immune surveillance.” Migration disorders of immune cells are related to autoimmune diseases, chronic inflammation, and tumor evasion. It is therefore essential to characterize immune cell motility in different physiologically and pathologically relevant scenarios to understand the regulatory mechanisms of functionality of immune responses. This review is focused on immune cell migration, to define the underlying mechanisms and the corresponding investigative approaches. We highlight the challenges that immune cells encounter in vivo, and the microfabrication methods to mimic particular aspects of their microenvironment. We discuss the advantages and disadvantages of the proposed tools, and provide information on how to access them. Furthermore, we summarize the directional cues that regulate individual immune cell migration, and discuss the behavior of immune cells in a complex environment composed of multiple directional cues.
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Smith, Robert E. "The Effects of Dietary Supplements that Overactivate the Nrf2/ARE System." Current Medicinal Chemistry 27, no. 13 (April 24, 2020): 2077–94. http://dx.doi.org/10.2174/0929867326666190517113533.
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Background: Inflammation is one of the most misunderstood aspects of human health. People have been encouraged to eat foods that have a high antioxidant capacity, and in vitro tests for total antioxidant capacity emerged. They were based on measuring the destruction of oxidized test compounds in direct reactions with the antioxidants in foods. Many dietary supplements arrived in the market. They contained purified antioxidants, such as resveratrol and EGCG that were and still are widely assumed by many to be quite healthy at any dose. Methods: The literature on inflammation and the Nrf2/ARE antioxidant system was searched systematically. Articles from prestigious, peer-reviewed journals were obtained and read. The information obtained from them was used to write this review article. Results: Over 150 articles and books were read. The information obtained from them showed that very few dietary antioxidants exert their effects by reacting directly with Reactive Oxygen and Nitrogen Species (RONS). Instead, most of the effective antioxidants activate the endogenous Nrf2/ARE antioxidant system. This helps prevent smoldering inflammation and the diseases that it can cause. However, when overactivated or activated constitutively, the Nrf2/ARE antioxidant system can cause some of these diseases, including many types of multidrug resistant cancer, autoimmune, neurodegenerative and cardiovascular diseases. Conclusion: Even though green tea, as well as many fruits, vegetables and spices are quite healthy, dietary supplements that deliver much higher doses of antioxidants may not be. People who are diagnosed with cancer and plan to start chemotherapy and/or radiotherapy should probably avoid such supplements. This is because multidrug resistant tumors can hijack and overactivate the Nrf2/ARE antioxidant system.
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Petta, Ioanna, Lien Dejager, Marlies Ballegeer, Sam Lievens, Jan Tavernier, Karolien De Bosscher, and Claude Libert. "The Interactome of the Glucocorticoid Receptor and Its Influence on the Actions of Glucocorticoids in Combatting Inflammatory and Infectious Diseases." Microbiology and Molecular Biology Reviews 80, no. 2 (May 11, 2016): 495–522. http://dx.doi.org/10.1128/mmbr.00064-15.
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SUMMARYGlucocorticoids (GCs) have been widely used for decades as a first-line treatment for inflammatory and autoimmune diseases. However, their use is often hampered by the onset of adverse effects or resistance. GCs mediate their effects via binding to glucocorticoid receptor (GR), a transcription factor belonging to the family of nuclear receptors. An important aspect of GR's actions, including its anti-inflammatory capacity, involves its interactions with various proteins, such as transcription factors, cofactors, and modifying enzymes, which codetermine receptor functionality. In this review, we provide a state-of-the-art overview of the protein-protein interactions (PPIs) of GR that positively or negatively affect its anti-inflammatory properties, along with mechanistic insights, if known. Emphasis is placed on the interactions that affect its anti-inflammatory effects in the presence of inflammatory and microbial diseases.
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Kalinin, R. E., I. A. Suchkov, N. D. Mzhavanadze, and N. V. Korotkova. "Endothelial dysfunction in muscular dystrophies." NAUKA MOLODYKH (Eruditio Juvenium) 9, no. 2 (June 30, 2021): 326–34. http://dx.doi.org/10.23888/hmj202192326-334.
Full textAbstract:
Endotheliocytes are the key elements of the vascular wall and are involved in regulation of vascular tone and permeability, inflammation, hemostasis, angiogenesis etc. Impaired function of endothelial cells universally recognized as endothelial dysfunction is associated with a number of common diseases such as ischemic heart disease, arterial hypertension, atherosclerosis, peripheral arterial disease, septic shock, chronic kidney disease, obesity, oncological and autoimmune diseases. Less is known about the role of endothelial cells in pathogenesis of development and progression of rare diseases, such as muscular dystrophies. Muscular dystrophies involve over 30 genetically determined diseases, which are characterized by the development of a progressive muscular weakness and skeletal muscle degeneration. Presence of a nucleotide variant associated with a certain muscular dystrophy is primarily marked by a limited potential of skeletal muscle regeneration due to the impaired structure and function of myogenic cells. Inherited myopathies include a group of severe neuromuscular diseases caused by a mutation in the dysferlin gene DYSF, which leads to the synthesis of a dysfunctional dysferlin. Complex molecular and cellular interactions involved in skeletal muscle damage and endothelial dysfunction play an important role in the pathogenesis of dysferlinopathies. The possibility to produce an effect on different pathological aspects of dysferlinassociated myopathies such as complement system activation, inflammation, impaired function of endothelial cells, damage and necrosis of myofibrils are extensively studied in vitro and in vivo. This article is dedicated to the current understanding of relationship between the endothelium and its dysfunction in myogenesis and skeletal muscle regeneration in normal and pathological conditions caused by a group of inherited progressive myodystrophies, dysferlinopathies in particular, as well as possible clinical application of endothelial cells in treatment of muscular dystrophies.
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Engin, Feyza. "ER stress and development of type 1 diabetes." Journal of Investigative Medicine 64, no. 1 (January 2016): 2–6. http://dx.doi.org/10.1097/jim.0000000000000229.
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Type 1 diabetes (T1D) results from an autoimmune-mediated destruction of pancreatic β cells. The incidence of T1D is on the rise globally around 3% to 5% per year and rapidly increasing incidence in younger children is of the greatest concern. currently, there is no way to cure or prevent T1D; hence, a deeper understanding of the underlying molecular mechanisms of this disease is essential to the development of new effective therapies. The endoplasmic reticulum (ER) is an organelle with multiple functions that are essential for cellular homeostasis. Excessive demand on the ER, chronic inflammation, and environmental factors lead to ER stress and to re-establish cellular homeostasis, the adaptive unfolded protein response (UPR) is triggered. However, chronic ER stress leads to a switch from a prosurvival to a proapoptotic UPR, resulting in cell death. Accumulating data have implicated ER stress and defective UPR in the pathogenesis of inflammatory and autoimmune diseases, and ER stress has been implicated in β-cell failure in type 2 diabetes. However, the role of ER stress and the UPR in β-cell pathophysiology and in the initiation and propagation of the autoimmune responses in T1D remains undefined. This review will highlight the current understanding and recent in vivo data on the role of ER stress and adaptive responses in T1D pathogenesis and the potential therapeutic aspect of enhancing β-cell ER function and restoring UPR defects as novel clinical strategies against this disease.
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Nachamkin, Irving, Ban Mishu Allos, and Tony Ho. "Campylobacter Species and Guillain-Barré Syndrome." Clinical Microbiology Reviews 11, no. 3 (July 1, 1998): 555–67. http://dx.doi.org/10.1128/cmr.11.3.555.
Full textAbstract:
SUMMARY Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.