Relevant bibliographies by topics / Molecular aspects of Autoimmune diseases

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Molecular aspects of Autoimmune diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Molecular aspects of Autoimmune diseases"

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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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Dissertations / Theses on the topic "Molecular aspects of Autoimmune diseases"

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Hall, Richard James, and n/a. "Chromosome 18 and autoimmune disease." University of Otago. Department of Biochemistry, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.141018.

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The autoimmune diseases embody a diverse range of common human conditions that are caused by a loss of self-tolerance in the host immune system to a specific organ or tissue type. Approximately 5% of the general population are affected by autoimmune diseases which include type 1 diabetes (T1D), rheumatoid arthritis (RA) and Graves disease (GD). The majority of the autoimmune diseases are multifactorial in origin, brought about by a combination of both environmental and genetic factors. Numerous susceptibility loci have been identified for each autoimmune disease and a number of these loci have been shown to be shared amongst the autoimmune diseases. The fine-mapping of susceptibility loci to the underlying disease genes remains the current challenge facing complex disease genetics. This project aimed to further characterise the autoimmune disease susceptibility locus IDDM6 on chromosome 18q12-21. This was achieved by using a comparative mapping approach that incorporates the study of genetic association in human autoimmune disease alongside the consomic mapping of the orthologous region in the non-obese diabetic (NOD) mouse model of autoimmunity. Deleted in colorectal carcinomas (DCC) provided a strong candidate gene at IDDM6 and the resident R201G polymorphism was identified as a functional candidate A potential mechanism for the R201G polymorphism involvement in T1D aetiology was identified where the polymorphism may affect the ability of DCC to induce apoptosis in vitro. However, no evidence for R201G association could be detected in autoimmune disease case-control datasets from the New Zealand (NZ) population (T1D n = 428, RA n = 730, autoimmune thyroid disease n = 192 (AITD); versus n = 1246 healthy controls). In addition, no evidence for R201G involvement in T1D could be provided in a transmission disequilibrium test (TDT) incorporating 382 affected sib-pair families (54.2% transmission; P = 0.15). Significant association of R201G with GD was detected in a United Kingdom (UK) dataset (P = 0.002) from the Newcastle population (423 cases vs. 393 controls) but this was not replicated in an additional dataset from the UK Birmingham population (731 cases vs 668 controls; P = 0.81). It was concluded that the R201G polymorphism may encode susceptibility to GD but is unlikely to be the sole aetiological variant that accounts for the linkage previously observed at IDDM6 in autoimmune disease. To further investigate DCC as a positional candidate at IDDM6, five SNPs were selected from a 100 kb window surrounding a DCC-resident microsatellite that had previously been associated with T1D, called "88,21". The five SNPs were genotyped in the NZ T1D dataset, and the ascertainment of estimated haplotypes in this dataset revealed association of a rare haplotype with T1D, called haplotype H (3.31% cases vs 1.17% controls; P = 0.0044), in addition to global association of all haplotypes (P = 0.018). Haplotype H was also associated in an independent case-control dataset from the UK comprised of 400 T1D subjects and 443 healthy controls (P = 0.038). Maximum support for association of haplotype H was extended when both the UK and NZ T1D datasets were combined (P = 0.0017). Association of haplotype H could not be verified in a family-based test for association using the 382 UK T1D families (P = 0.40). However, the inclusion of the DCC SNPs in a TDT analysis of the published DCC-resident microsatellites "88,21" and "55,26", that had been used to identify IDDM6, extends support for the previously-associated 2-10 haplotype (2-10 refers to the published allele nomenclature at "88,21" and "55,26" respectively; 2-10-haplotype A; 59.6% T; P = 0.0058). There was no evidence for association of the five SNPs with RA or AITD when using either individual SNP analyses or estimated haplotypes in the NZ datasets. A similar lack of association was reported for the UK Newcastle GD dataset. Taken together, these data further support DCC, or a nearby gene, as conferring susceptibility to T1D. The human genetic data that supports IDDM6 involvement in autoimmune disease is further strengthened by consomic mapping of the orthologous region in mouse, using the non-obese diabetic mouse (NOD) model of autoimmune disease. In this thesis, the first evidence for a diabetes and thyroiditis susceptibility locus on mouse chromosome 18 is presented, which have been designated Idd21 and Sat1 respectively. This was achieved by using a chromosome-replacement strain with chromosome 18 derived from the diabetes-resistant Biozzi ABH strain on a diabetes-susceptible NOD genome, called NOD.ABH[Chr�⁸]. Mouse chromosome 18 contains orthology to both IDDM6 and the rat diabetes-susceptibility locus Iddm3. The NOD.ABH[Chr�⁸] mice showed a dramatic and significant reduction in diabetes incidence (30% of females were affected by 7 months of age versus 85% in NOD; P <0.0001) and that of thyroiditis (15.5% at 12 months compared to 37.4% in NOD; P <0.002). The comparative mapping of the chromosome 18 autoimmune susceptibility locus IDDM6 in human and mouse presented in this thesis provides further support for this locus. This research also clearly defines the next steps required to fine-map IDDM6 to the underlying disease genes, especially in regard to the DCC gene.
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Yang, Min, and 杨敏. "Role of regulatory B cells in autoimmune disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48079832.

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Although B cells are well-known for their functions in antibody production and antigen presentation, certain B cell subsets have been recently identified as regulatory B cells to modulate immune responses through cytokine production. However, the microenvironmental factors involved in the induction of regulatory B cells remain largely uncharacterized. B cell-activating factor (BAFF), a member of TNF family cytokines produced by myeloid cells, is a key regulator for B cell maturation and function. However, it remains unknown whether BAFF plays a role in modulating the generation of regulatory B cells and how regulatory B cells suppress autoimmune pathogenesis. In this study, treatment with BAFF significantly increased IL-10-producing B cells in culture of mouse splenic B cells, an effect specifically abrogated by neutralization with TACI-Fc. BAFF-induced IL-10-producing B cells showed a distinct CD1dhiCD5+(B10) phenotype. Phenotypic analysis further indicated that these BAFF-induced B10 cells were marginal-zone (MZ)-like B cells. Interestingly, BAFF treatment in vivo also increased the number of IL-10-producingB cells in splenic MZ regions. Moreover, chromatin immunoprecipitation analysis revealed that BAFF activated the transcription factor AP-1 for binding to IL-10 promoter, demonstrating a novel function for BAFF in inducing IL-10 production. Furthermore, those BAFF-induced B10 cells exhibited significant suppressive effects on CD4+T cell proliferation and Th1 cytokine production in culture. To explore whether these BAFF-induced B10 cells possess a regulatory function in suppressing autoimmune progression in vivo, collagen-induced arthritis (CIA) mouse model was employed. In vitro-expanded B10 cells and other control B cells were intravenously transferred into DBA/1J mice on the day of 2ndcollagen II (CII)-immunization. After adoptive transfer of BAFF-induced B10 cells, CII-immunized mice exhibited a delayed onset of arthritis and substantially reduced severity of clinical symptoms. The pathogenesis of IL-17-producing CD4+T cells (Th17) in the development of arthritis has been well-recognized, which has led me to test the hypothesis whether B10 cells ameliorate the development of arthritis via modulating Th17 cells. During the progression of CIA, IL-10-producing B cells were decreasedwhereasTh17 cells were significantly increased at the acute phase of CIA. Upon transfer of BAFF-induced B10 cells, a substantially reduction ofTh17 cells in both lymphoid organs and inflamed joints were detected. To verify whether B10 cells inhibit Th17 cell generation in culture, CFSE-labeled na?ve CD4+T cells were cocultured with B10 cells in Th17 cell polarization medium. It was found that B10 cells suppressed Th17 cell differentiation via reducing STAT3 phosphorylation and RORt expression. Although adoptive transfer of Th17 cells triggered the development of CIA in IL-17-/-DBA mice, cotransfer of B10 cells with Th17 cells profoundly delayed the onset of delayed the onset of arthritisand remarkably reduced the infiltration of Th17 cells in synovial fluid. Taken together, I have identified a novel function of BAFF in the induction of IL-10-producing regulatory B cells. My findings that adoptive transfer of BAFF-expanded B10 cells can effectively suppress the development of experimental arthritisin mice via the inhibition of Th17 cell generation may contribute to the development of new therapeutic strategies in treating human rheumatoid arthritis.
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Pathology
Doctoral
Doctor of Philosophy
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Hollis-Moffatt, Jade Elissa, and n/a. "Fine mapping and characterisation of an autoimmune diabetes locus, insulin dependent diabetes 21, (Idd21) on mouse chromosome-18." University of Otago. Department of Biochemistry, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070130.151657.

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Autoimmune disease is comprised of a wide variety of disorders characterised by a loss of self-tolerance towards a target organ or systemic region leading to its eventual destruction. Type 1 diabetes (T1D), autoimmune thyroid disease (AITD) and inflammatory bowel disease (IBD) are debilitating organ-specific disorders. These disorders arise from a combination of genetic factors and environmental triggers. A greater level of basic understanding of these disorders is required to delay and/or prevent their effects. Numerous autoimmune susceptibility loci have been implicated in the development of these disorders, but only a few causative genes have been identified. The aim of this project was to use comparative mapping between the human and mouse genomes to provide a greater understanding of the human autoimmune susceptibility locus, IDDM6, shown to be involved in a number of autoimmune disease conditions. Hall et al., (2003) previously demonstrated that the mouse autoimmune diabetes locus, Idd21, on distal mouse chr18 contains orthology to human IDDM6, IDDM10, IDDM18 and rat Iddm3. As part of this project the Idd21 locus was fine mapped using the congenic mapping technique. Beginning with the consomic mouse strain, NOD.ABHChr18 (90Mb of Biozzi/ABH-derived diabetes-resistant chr18 introgressed onto a non-obese diabetic (NOD) genetic background), 13 NOD.ABHIdd21 congenic mouse strains were established. The diabetes incidences of these congenic mouse strains were statistically compared stepwise along mouse chr18 and Idd21 was fine mapped to at least four independent autoimmune diabetes loci. Idd21.1 and Idd21.2 were located on distal mouse chr18 in regions orthologous to human IDDM6 and rat Iddm3 and Idd21.3a/b and Idd21.4 were located on proximal mouse chr18 in regions orthologous to human IDDM18 and IDDM10 respectively. Candidate genes of notable interest include Map3k8, Spink5, Cd14, Dcc, Smad4 and 7, Miz1, Nfatc1 and Cd226. Idd21.1 was further fine mapped. Beginning with the NOD.ABHD18Mit8-D18Mit214[(75-85.1Mb)] (Idd21.1) congenic strain (containing at least 10.1Mb of distal chr18 Biozzi/ABH diabetes-resistant DNA introgressed onto a NOD genetic background), seven subcongenic mouse strains were created. The diabetes incidence of these subcongenic mouse strains were statistically compared stepwise along mouse chr18 and Idd21.1 was fine mapped to at least three independent autoimmune diabetes loci; Idd21.11 (72.6-76.1Mb), Idd21.12a/b (75-76.1Mb and 80.6-81.4Mb) and Idd21.13 (84.8-85.1Mb). Candidate genes of interest in these regions include Dcc, Smad4 and 7, Miz1, Nfatc1, and Cd226. Functional characterisation of the Idd21.1 locus was performed by adoptively transferring splenocytes from female NOD or NOD.ABHIdd21.1 mice into cohorts of severe combined immune deficient (scid) female mice, NOD/LtSz.Prkdc[scid] and NOD/LtSz.Prkdc[scid].ABHIdd21.1. There were two notable findings from this work. Firstly, NOD.ABHIdd21.1 splenocytes are not as effective as NOD at transferring diabetes to either NOD/LtSz.Prkdc[scid] (P = 0.0004) or NOD/LtSz.Prkdc[scid].ABHIdd21.1 (P = 0.0178), suggesting that Idd21.1 acquired immune cells are not as diabetogenic as NOD. Secondly, NOD/LtSz.Prkdc[scid].ABHIdd21.1 mice are more resistant to autoimmune attack than NOD/LtSz.Prkdc[scid] when injected with either NOD (P = 0.0015) or NOD.ABHIdd21.1 splenocytes (P = 0.0014), suggesting that Idd21.1 either acts by altering the intrinsic resistance of beta-cells to autoimmune attack or due to changes in the innate immune system. Other NOD-based models of autoimmune disease, spontaneous and experimental autoimmune thyroiditis and spontaneous colitis, were also investigated to determine whether Idd21.1 is a common autoimmune disease locus. When bred onto the NOD.Cg-H2[h4] (thyroiditis model) genetic background Idd21.1 was demonstrated to increase the development of thyroiditis and reduce the incidence of insulitis in spontaneous (untreated) but not experimental (NaI-induced) NOD.Cg-H2[h4] mice. When bred onto the NOD.Cg-Il10[tm1Cgn] (colitis) genetic background Idd21.1 was demonstrated to inhibit the development of rectal prolapse in breeding female NOD.Cg-Il10[tm1Cgn] mice. Data from this thesis demonstrate that the IDDM6 orthologous region in mouse, Idd21.1, contains several loci that influence autoimmune diabetes, thyroiditis and colitis in NOD-based mouse models. These findings are consistent with previous knowledge that IDDM6 is a common autoimmune susceptibility locus.
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Narayanan, Harish Anandha. "Molecular Understanding of Selected Autoimmune Diseases." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146614.

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Pathogens that affect the immune system, or defects in the immune system contribute to numerous autoimmune diseases. In this paper, we are going to review, analyze and understand recent findings in literature. The papers that are to be reviewed explore the observation of loss of regulatory T cells in individuals with multiple sclerosis, the importance of CD4+ during HIV infection, the role of CCR6 in the immune system and the importance of Pan-DR-Binding Hsp60 self-epitopes in rheumatoid arthritis. So this literary review is limited to understanding major defects in specific parts of the immune system and its role in causing the specific autoimmune disease. The reason for this focus is to highlight the importance of the immune system in the functioning of many processes in our body and more specifically the importance of T cells and its regulators in maintaining the immune system.
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Halonen, Maria. "Monogenic model for autoimmune diseases : molecular basis of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED)." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/halonen/.

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Tam, Chun-yee, and 譚雋怡. "Dissecting the physiological role of the novel lupus-associated C-type lectin-like protein CLEC16A." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206749.

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The CLEC16A locus has been identified as a susceptibility gene for multiple autoimmune diseases, including multiple sclerosis, type-I diabetes and systemic lupus erythematosus (SLE), in genome-wide association studies. CLEC16A encodes a novel C-type lectin-like protein, by virtue of a predicted C-type lectinlike domain (CTLD), with unclear function. Studies on the disease-associated SNPs have suggested that CLEC16A polymorphisms affect the expression of neighboring genes, while the effect on its own expression is unclear. Several functional studies have interrogated the physiological role(s) of CLEC16A in disparate directions. The Drosophila ortholog of CLEC16A, Ema, has been reported to regulate endosomal protein trafficking and the autophagic process, while CLEC16A has been found to participate in LPS-induced inflammatory cytokine response in rat astrocytes. Since there is not a consenting role ascribed to CLEC16A, this study was undertaken to investigate the functional involvement(s) of CLEC16A in mammalian cells and the expression of CLEC16A in lupus patients, with the attempt to comprehend the association between CLEC16A and SLE. By overexpressing in non-immune epithelial cells, CLEC16A was revealed to be an intracellular protein of ~130 kDa in size. CLEC16A displayed a punctated expression pattern, which did not co-localize with endosomes, lysosomes, autophagosomes or endoplasmic reticulum in steady state. When treated with rapamycin or serum-starved, CLEC16A-overexpressing cells exhibited a reduced autophagic response, suggesting that CLEC16A may have an inhibitory role in autophagy. Besides the predicted CTLD, motif prediction has also implicated an immunomodulatory role for CLEC16A. Due to the observed inhibition on autophagy, coupled with recent findings linking autophagy and inflammasome activation, the involvement of CLEC16A in NLRP3 inflammasome was investigated. By knocking down CLEC16A in the human macrophage-like THP-1 cells, CLEC16A was found to potentially regulate NLRP3 inflammasome activation via inhibiting the LPS-induced pro-IL-1aasynthesis. Finally, the expressions of the long and short isoforms, CLEC16A_V1 and CLEC16A_V2 of CLEC16A in PBMCs were compared between healthy controls and SLE patients. A higher CLEC16A_V1 expression was observed in SLE patients, whereas the reverse was found for CLEC16A_V2. The expressions of the isoforms, however, were not correlated with the disease severity and clinical manifestations. The finding that CLEC16A may inhibit autophagy is in contrast with the reported function of Ema in supporting autophagy, and such discrepancy could be because of the different cell systems used. The finding that CLEC16A may downregulate NLRP3 inflammasome activation has not been previously reported, and the mechanism(s) of such regulation warrant(s) future studies. The molecular basis of how CLEC16A regulates autophagy and inflammasome waits to be delineated. Such knowledge, together with information of where endogenous CLEC16A is expressed, shall incite better understanding of the contribution of CLEC16A to SLE development.
published_or_final_version
Medicine
Doctoral
Doctor of Philosophy
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Mulcahy, Anthony Francis. "The molecular cloning and characterisation of autoantigens." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242453.

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龔慧慈 and Wai-chee Annie Kung. "Thyroglobulin gene expression and thyroid functions in health and autoimmune thyroid diseases." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1990. http://hub.hku.hk/bib/B31981355.

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Ye, Ping. "Autoimmunity in chronic periodontitis." University of Sydney, 2003. http://hdl.handle.net/2123/4256.

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Abstract:
Doctor of Philosophy
Profound perturbation of epithelial structure is a characteristic feature of the immunopatholoical response to bacterial antigens considered to be central in the pathogenesis of the destructive lesion of periodontitis. The pathological basis for the disturbance of epithelial structure is not understood. It was demonstrated that the structural integrity and functional differentiation of the lining epithelium is compromised in relation to inflammatory changes associated with destructive periodontitis. In the pathological lining epithelium of the periodontal pocket there was a marked reduction of epithelial cadherin important in intercellular adhesion, of involucrin, a marker of terminal differentiation, and of the gap junction connexions that form intercellular communication channels. These changes were associated with alterations of filamentous actin expression, collectively indicating profound perturbation of epithelial structure. The data reported support the concept that the ability of the pathological lining epithelium to function as an effective barrier against the ingress of microbial products into the tissues is severely compromised (Ye et al., 2000). In addition, a recent study (Ye et al., 2003) by Western analysis of serum IgG from all 22 patients with chronic periodontitis tested indicated recognition of multiple epithelial components in individual patterns. In contrast, subjects with a healthy periodontium displayed only trace recognition of epithelial antigens. Levels of epithelial-reactive antibodies were significantly correlated with attachment loss as an indication of disease activity. To investigate a possible relationship between the bacterial flora adjacent to the diseased sites and the presence of epithelial-reactive antibodies, subgingival plague samples were taken from deep periodontal pockets and cultured anaerobically. Gram positive bacteria containing antigens potentially cross-reactive with epithelial cells were reproducibly isolated by probing membrane colony lifts with affinity-isolated (epitheial-specific) antibodies. The bacteria were identified as streptococci (S. mitis, S. constellatus and two S. intermedius strains) and Actinomyces (A. georgiae, and A. sp. oral clone) by 16S rDNA sequence homology. Recognition by affinity-isolated antibodies of antigens from the captured organisms was confirmed by Western analysis. Conversely, absorption of affinity-isolated antibodies with bacterial species specifically reduced subsequent recognition of epithelial antigens. To identify the auto-antigens, a human keratinocyte cDNA expression library in Lambda phage was probed using a pooled sera. Groups of responders were detected for CD24 (a recently described adhesion molecule also known as P-selectin ligand), antioxidant protein 2 (a newly recognised member of the thiol-dependment anti-oxidant proteins), lavtate dehydrogenase A, the transcription factor NFAT5, and for three genes encoding novel proteins. Six identified bacteria, especially S intermedius were demonstrated to absorb antibodies reaching with identified auto-antigens in patterns varying between individuals. This evidence indicated that during the course of periodontits, subjects develop increased levels of antibodies to common oral bacteria amongst which are included tissue cross-reactive antigens. Periodontitis could therefore present a risk for the subsequent initiation or exacerbation of a broad spectrum of disease processes including autoimmune, inflammatory, proliferative and degenerative disorders.
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Silver, Karlee Linnea. "Genotypic and phenotypic approaches to pathways involved in humoral autoimmunity." Thesis, University of Oxford, 2006. http://ora.ox.ac.uk/objects/uuid:1a18398f-942a-49a4-bd2e-a8ec4b4f647f.

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Books on the topic "Molecular aspects of Autoimmune diseases"

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1957-, Demaine Andrew G., Banga J.-Paul 1953-, McGregor Alan M. 1948-, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. The molecular biology of autoimmune disease. Berlin: Springer-Verlag, 1990.

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Conrad, K. Autoantibodies in systemic autoimmune diseases: A diagnostic reference. Lengerich: Pabst Science Pub., 2002.

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George, Kahaly, ed. Endocrine ophthalmopathy: Molecular, immunological and clinical aspects. Basel: Karger, 1993.

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NATO Advanced Research Workshop on Fundamental and ExperimentalAspects of Autoimmunity (1993 Acquafredda di Maratea, Italy). Autoimmunity: Experimental aspects. Berlin: Springer-Verlag in cooperation with NATO Scientific Affairs Division, 1994.

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International Association of Biomedical Gerontology. International Congress. Molecular mechanisms and models of aging. Boston: Blackwell Pub. on behalf of the New York Academy of Sciences, 2007.

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Weetman, Anthony P. Autoimmune endocrine disease. Cambridge: Cambridge University Press, 1991.

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A, McCombe Pamela, ed. Autoimmune neurological disease. Cambridge: Cambridge University Press, 1995.

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Epigenetic contributions in autoimmune disease. New York: Springer Science+Business Media, 2011.

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Hertl, Michael. Autoimmune diseases of the skin: Pathogenesis, diagnosis, management. 3rd ed. Wien: Springer, 2011.

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Becker, Yechiel, Gholamreza Darai, and Eng-Shang Huang, eds. Molecular Aspects of Human Cytomegalovirus Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6.

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Book chapters on the topic "Molecular aspects of Autoimmune diseases"

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Hughes, Travis, and Amr H. Sawalha. "Autoimmune Diseases." In Epigenetic Aspects of Chronic Diseases, 95–106. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-644-1_6.

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Edwards, N. Lawrence. "Autoimmune Diseases." In Principles of Molecular Medicine, 299–307. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_34.

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Khan, Ashraf, and Otto Walter. "Autoimmune Thyroid Diseases." In Molecular Pathology Library, 37–45. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-1707-2_5.

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Wayne, Sigrid. "Systematic Autoimmune Diseases." In Molecular Pathology Library, 9–19. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-1707-2_2.

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Chen, Youhai H. "Apoptosis and Autoimmune Diseases." In Molecular Mechanisms of Programmed Cell Death, 67–78. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-5890-0_6.

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Coppedè, Fabio, and Lucia Migliore. "Epigenetics of Autoimmune Diseases." In Molecular mechanisms and physiology of disease, 151–73. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0706-9_6.

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Williams, D. M., and D. Wray. "Autoimmune Mucocutaneous Diseases and Diseases of Uncertain Aetiology." In Immunological Aspects of Oral Diseases, 125–48. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4167-0_6.

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Spiteri, Monica A., and Graham A. W. Rook. "The Lung in Granulomatous Diseases." In Autoimmune Aspects of Lung Disease, 87–109. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8926-1_4.

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Rapti, Angela, Beratha S. Devi, Stephen G. Spiro, and David A. Isenberg. "The Respiratory System in Rheumatic Diseases." In Autoimmune Aspects of Lung Disease, 23–51. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8926-1_2.

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Tsuruta, Daisuke, Teruki Dainichi, Takahiro Hamada, Norito Ishii, and Takashi Hashimoto. "Molecular Diagnosis of Autoimmune Blistering Diseases." In Methods in Molecular Biology, 17–32. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-227-8_2.

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Conference papers on the topic "Molecular aspects of Autoimmune diseases"

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Barturen, G., M. Kerick, D. Alvarez-Errico, R. Quintares, E. Carnero, D. Gemperline, E. Dow, et al. "S1A:5 Molecular stratification of autoimmune diseases based on epigenetic profiles." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.2.

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Barturen, Guillermo, Sepideh Babaei, Francesc Català-Moll, Manuel Martínez-Bueno, Zuzanna Makowska, Jordi Martorell-Marugán, Pedro Carmona-Sáez, et al. "O31 Integrative analysis reveals a molecular stratification of systemic autoimmune diseases." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.42.

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Pshenichnaya, N. Yu, I. A. Lizinfeld, G. Yu Zhuravlev, and N. S. Morozova. "CHARACTERISTICS OF INCIDENCE RATE OF COVID-19, ACUTE RESPIRATORY DISEASES, INFLUENZA AND COMMUNITY ACQUIRED PNEUMONIA IN RUSSIA ACCORDING TO CLIMATE, GEOGRAFICAL ASPECTS AND POPULATION DENSITY." In Molecular Diagnostics and Biosafety. Federal Budget Institute of Science 'Central Research Institute for Epidemiology', 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-184.

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Yoshimoto, K., K. Suzuki, K. Sugahara, and T. Takeuchi. "THU0055 Low molecular weight baff signaling inhibitors ameliorate IL-6, IL-10 and IGG production in vitro and in vivo models of autoimmune diseases." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4176.

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