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Artykuły w czasopismach na temat "Apoptosis Immunological aspects"
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Kokron, Cristina M., Paolo R. Errante, Myrthes T. Barros, Gisele V. Baracho, Maristela M. Camargo, Jorge Kalil, and Luiz V. Rizzo. "Clinical and laboratory aspects of common variable immunodeficiency." Anais da Academia Brasileira de Ciências 76, no. 4 (December 2004): 707–26. http://dx.doi.org/10.1590/s0001-37652004000400007.
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Common variable immunodeficiency (CVID) is an immunological disorder characterized by defective antibody production, recurrent infections, most notably of the respiratory tract, autoimmune phenomena and cancer. Some CVID patients may also present disturbances of the cellular immune response such as a decrease in the number and proportion of different lymphocyte populations, diminished lymphoproliferative response to mitogens and antigens, altered production of cytokines, and deficient expression of cell-surface molecules. Most Brazilian CVID patients included in this study show a decrease in T and B lymphocyte counts in the peripheral blood. Furthermore, their lymphocytes are more susceptible to apoptosis following activation than normal individuals, and they have a decrease in the expression of activation molecules like CD25, CD69, CD40L and CD70. Moreover, they show a decreased synthesis of IL-4 and IL-5 in comparison with normal individuals. The increase in susceptibility to apoptosis following activation, may also be responsible for the decrease in the expression of activation molecules and CD40L, decrease in Th2 cytokines synthesis, and in the number of T and B circulating cells. In this study we discuss some of these immunological disturbances correlating them to the patients' clinical features and comparing our patients' findings to the literature.
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SALIKHOVA, T. R., N. S.-M. OMAROV, A. U. CHERKESOVA, S. M. GADJIMURADOVA, and E. R. ASKERKHANOVA. "CLINICO-MORPHOLOGICAL AND IMMUNOHISTOCHEMICAL ASPECTS OF ENDOMETRIAL POLYP PATHOGENESIS IN POSTMENOPAUSE." Periódico Tchê Química 16, no. 32 (August 20, 2019): 724–31. http://dx.doi.org/10.52571/ptq.v16.n32.2019.742_periodico32_pgs_724_731.pdf.
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To study hypoxia-inducible transcription factor HIF-1α expression in endometrial polyps (EP) considering their clinical-morphological and immunological features during postmenopause. A complex clinical and laboratory examination of 120 postmenopausal patients was carried out. 90 of them developed EP, whereas 30 had morphologically unchanged endometrium. Immune histochemical (ICH) testing was used to evaluate HIF-1α expression in epithelial and stromal cells of polyps in adjacent and control endometrium. A complex of the most significant risk factors in EP genesis such as high rate of inflammatory disorders of genital organs (IDGO), extragenital, metabolic and endocrine disorders and intrauterine contraception (IUC) was found. High expression of HIF-1α in epithelial cells and in the area of inflammatory infiltrate of glandular fibrous EP stroma was established as compared with control endometrium. HIF-1α expression in epithelial cells and in the area of inflammatory infiltrate of EP glandular fibrous stroma against the background of inflammatory, metabolic and endocrine, immunological changes and age-related involutional processes indicated local hypoxia. Epigenetic changes can develop in the processes of proliferation and apoptosis and in the processes that control neoplastic transformation. The obtained data can provide grounds for patient-tailored EP therapy in postmenopausal patients.
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PASSOS, ELIANA M. DOS, VALÉRIA WANDERLEY-TEIXEIRA, EDMILSON J. MARQUES, ÁLVARO A. C. TEIXEIRA, and FÁBIO A. BRAYNER. "Cotesia flavipes (CAM) (Hymenoptera: Braconidae) Supresses Immune Responses In Diatraea flavipennella (BOX) (Lepidoptera: Crambidae)." Anais da Academia Brasileira de Ciências 86, no. 4 (December 2014): 2013–24. http://dx.doi.org/10.1590/0001-3765201420130393.
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The present research aimed to elucidate which aspects of immune responses in Diatraea flavipennella are suppressed by the parasitoid Cotesia flavipes, thus, ensuring parasitism success. We investigated the presence of apoptosis in fat body cells through the TUNEL technique. According to the results, reduced levels of nitric oxide and phenoloxidase activity were observed in larvae parasitized for three days, and reduced total number of hemocytes, after three and seven days. An increase in plasmatocytes and decrease in spherulocytes numbers were observed in the differential count on the third day of parasitism. The number of melanized microspheres in parasitized larvae was low and indicated less intense melanization. The ultrastructural analysis confirmed the immunosuppressive effect of C. flavipes on the encapsulation response of D. flavipennella because only the formation of hemocytes capsules, adhered to the microspheres' surface, was evidenced in non-parasitized caterpillars. The effect of parasitism was also recorded on the third day with the presence of hemocytes and apoptosis in fat body cells, including aspects of degeneration in the latter. We concluded that C. flavipes suppresses cellular and humoral immunological responses in D. flavipennella and drastically affects the host's fat tissue.
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Signorile, Anna, Anna Ferretta, Maddalena Ruggieri, Damiano Paolicelli, Paolo Lattanzio, Maria Trojano, and Domenico De Rasmo. "Mitochondria, Oxidative Stress, cAMP Signalling and Apoptosis: A Crossroads in Lymphocytes of Multiple Sclerosis, a Possible Role of Nutraceutics." Antioxidants 10, no. 1 (December 28, 2020): 21. http://dx.doi.org/10.3390/antiox10010021.
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Multiple sclerosis (MS) is a complex inflammatory and neurodegenerative chronic disease that involves the immune and central nervous systems (CNS). The pathogenesis involves the loss of blood–brain barrier integrity, resulting in the invasion of lymphocytes into the CNS with consequent tissue damage. The MS etiology is probably a combination of immunological, genetic, and environmental factors. It has been proposed that T lymphocytes have a main role in the onset and propagation of MS, leading to the inflammation of white matter and myelin sheath destruction. Cyclic AMP (cAMP), mitochondrial dysfunction, and oxidative stress exert a role in the alteration of T lymphocytes homeostasis and are involved in the apoptosis resistance of immune cells with the consequent development of autoimmune diseases. The defective apoptosis of autoreactive lymphocytes in patients with MS, allows these cells to perpetuate, within the CNS, a continuous cycle of inflammation. In this review, we discuss the involvement in MS of cAMP pathway, mitochondria, reactive oxygen species (ROS), apoptosis, and their interaction in the alteration of T lymphocytes homeostasis. In addition, we discuss a series of nutraceutical compounds that could influence these aspects.
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Nicola, Monica-Georgiana, Liliana Mocanu, Aritina Elvira Morosanu, Sorin Berbece, and Loredana Elena Stoica. "The Immunohistochemical Expression of Bcl2, Ki 67and CD3 correlated with the Basal Cell Carcinoma Histological Features - a study on 10 cases." Revista de Chimie 71, no. 1 (February 7, 2020): 249–53. http://dx.doi.org/10.37358/rc.20.1.7841.
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The basal cell carcinoma represents a worldwide major health problem due to incidence, functional and aesthetical defects which accompanies the disease and its treatment and high recurrency risk.The various morphoclinical forms of the basal cell carcinoma may be explained due to at least three factors: genetical predisposal, the individual immunological status and the action of the risk factors. In the case in which the histological aspects do present some modifications which cannot be catalogued in the usual patterns, therefore inseriated sections of the hole tumor being imposed, in order to establish correctly the diagnosis and in the case in which microscopical criteria are partially overposable with those specific to another lesion, the immunohistochemical evaluation is imposed.The immunohistochemical studies are also used in research, thus revealing some biological aspects of the basal cell carcinoma. The study of the biological markers of the apoptosis, cellullarproliferation and the immunitary system reaction allows the understanding of the morphofunctional anomalies during the neoplastic transformation process and the early identification of the aggressive forms.
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Yamamoto, Toshiyuki, and Ichiro Katayama. "Vascular Changes in Bleomycin-Induced Scleroderma." International Journal of Rheumatology 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/270938.
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Systemic sclerosis (SSc) is characterized by vascular injury, immunological abnormalities, and fibrosis of the skin as well as various internal organs. Vascular impairment is the early manifestation and plays a fundamental role in the pathogenesis of SSc. Recent studies suggest that complex interactions among the endothelial cells, pericytes, smooth muscle cells, and fibroblasts are involved in the systemic vasculopathy in SSc, and histological feature of proliferation of vascular wall is seen in the lesional scleroderma skin at the late stage of disease. One of the most representative mouse models for scleroderma is the bleomycin-induced scleroderma; however, aspects of vascular alteration have not been described in detail so far. A number of studies have shown that bleomycin stimulates endothelial cells and fibroblasts to induce proinflammatory and fibrogenic cytokines, apoptosis, reactive oxygen species, and so on. This paper makes a focus on the vascular involvement in the bleomycin-induced murine scleroderma.
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Zivadinovic, Radomir, Aleksandra Petric, Goran Lilic, Vekoslav Lilic, and Biljana Djordjevic. "Persistent human papillomavirus infection in the etiology of cervical carcinoma: The role of immunological, genetic, viral and cellular factors." Srpski arhiv za celokupno lekarstvo 142, no. 5-6 (2014): 378–83. http://dx.doi.org/10.2298/sarh1406378z.
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The aim of this paper was to present the role of human papillomavirus (HPV) in cervical carcinogenesis from several aspects. By explaining the HPV virus lifecycle and structure, its effect on cervical cell cycle and subversion of immune response can be better understood. Early E region of the viral genome encodes proteins that are directly involved in carcinogenesis. The E6 protein binds to p53 protein (product of tumor-suppressor gene) blocking and degrading it, which in turn prevents cell cycle arrest and apoptosis induction. E6 is also capable of telomerase activation, which leads to cell immortalization; it also reacts with host proto-oncogene c-jun, responsible for transcription, shortens G1 phase and speeds up the transition from G1 to S phase of the cells infected by HPV. E7 forms bonds with retinoblastoma protein (product of tumor-suppressor gene) and inactivates it. It can inactivate cyclin inhibitors p21, p27, and abrogate the mitotic spindle checkpoint with the loss of protective effect of pRB and p53. The immune system cannot initiate early immunological reaction since the virus is non-lytic, while the concentration of viral proteins - antigens is low and has a basal intracellular position. Presentation through Langerhans cells (LC) is weak, because the number of these cells is low due to the effect of HPV. E7 HPV reduces the expression of E-cadherin, which is responsible for LC adhesion to HPVtransformed keratinocytes. Based on these considerations, it may be concluded that the process of cervical carcinogenesis includes viral, genetic, cellular, molecular-biological, endocrine, exocrine and immunological factors.
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Brandler, Samantha, Alice Lepelley, Marion Desdouits, Florence Guivel-Benhassine, Pierre-Emmanuel Ceccaldi, Yves Lévy, Olivier Schwartz, and Arnaud Moris. "Preclinical Studies of a Modified Vaccinia Virus Ankara-Based HIV Candidate Vaccine: Antigen Presentation and Antiviral Effect." Journal of Virology 84, no. 10 (March 10, 2010): 5314–28. http://dx.doi.org/10.1128/jvi.02329-09.
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ABSTRACT Poxvirus-based human immunodeficiency virus (HIV) vaccine candidates are currently under evaluation in preclinical and clinical trials. Modified vaccinia virus Ankara (MVA) vectors have excellent safety and immunogenicity records, but their behavior in human cell cultures remains only partly characterized. We studied here various virological and immunological aspects of the interactions of MVA-HIV, a vaccine candidate developed by the French National Agency for AIDS Research (ANRS), with primary human cells. We report that MVA-HIV infects and drives Gag expression in primary macrophages, dendritic cells (DCs), and epithelial and muscle cells. MVA-HIV-infected DCs matured, efficiently presented Gag, Pol, and Nef antigens, and activated HIV-specific cytotoxic T lymphocytes (CTLs). As expected with this type of vector, infection was cytopathic and led to DC apoptosis. Coculture of MVA-HIV-infected epithelial cells or myotubes with DCs promoted efficient Gag antigen major histocompatibility complex class I (MHC-I) cross-presentation without inducing direct infection and death of DCs. Antigen-presenting cells (APCs) infected with MVA-HIV also activated HIV-specific CD4+ T cells. Moreover, exposure of DCs to MVA-HIV or to MVA-HIV-infected myotubes induced type I interferon (IFN) production and inhibited subsequent HIV replication and transfer to lymphocytes. Altogether, these results show that MVA-HIV promotes efficient MHC-I and MHC-II presentation of HIV antigens by APCs without facilitating HIV replication. Deciphering the immune responses to MVA in culture experiments will help in the design of innovative vaccine strategies.
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Sochacka-Ćwikła, Aleksandra, Andrzej Regiec, Michał Zimecki, Jolanta Artym, Ewa Zaczyńska, Maja Kocięba, Iwona Kochanowska, Iwona Bryndal, Anna Pyra, and Marcin Mączyński. "Synthesis and Biological Activity of New 7-Amino-oxazolo[5,4-d]Pyrimidine Derivatives." Molecules 25, no. 15 (August 4, 2020): 3558. http://dx.doi.org/10.3390/molecules25153558.
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The synthesis of a series of novel 7-aminooxazolo[5,4-d]pyrimidines 5, transformations during their synthesis and their physicochemical characteristics have been described. Complete detailed spectral analysis of the intermediates 2–4, the N′-cyanooxazolylacetamidine by-products 7 and final compounds 5 has been carried out using MS, IR, 1D and 2D NMR spectroscopy. Theoretical research was carried out to explain the privileged formation of 7-aminooxazolo[5,4-d]pyrimidines in relation to the possibility of their isomer formation and the related thermodynamic aspects. Additionally, the single-crystal X-ray diffraction analysis for 5h was reported. Ten 7-aminooxazolo[5,4-d]pyrimidines 5 (SCM1–10) were biologically tested in vitro to preliminarily evaluate their immunological, antiviral and anticancer activity. Compounds SCM5 and SCM9 showed the best immunoregulatory profile. The compounds displayed low-toxicity and strongly inhibited phytohemagglutinin A-induced proliferation of human peripheral blood lymphocytes and lipopolysaccharide-induced proliferation of mouse splenocytes. Compound SCM9 caused also a moderate suppression of tumor necrosis factor α (TNF-α) production in a human whole blood culture. Of note, the compounds also inhibited the growth of selected tumor cell lines and inhibited replication of human herpes virus type-1 (HHV-1) virus in A-549 cell line. Molecular investigations showed that the compounds exerted differential changes in expression of signaling proteins in Jurkat and WEHI-231 cell lines. The activity of SCM5 is likely associated with elicitation of cell signaling pathways leading to cell apoptosis. The compounds may be of interest in terms of therapeutic utility as inhibitors of autoimmune disorders, virus replication and antitumor agents.
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Merani, Shaheed, and A. M. James Shapiro. "Current status of pancreatic islet transplantation." Clinical Science 110, no. 6 (May 15, 2006): 611–25. http://dx.doi.org/10.1042/cs20050342.
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DM (diabetes mellitus) is a metabolic disorder of either absolute or relative insulin deficiency. Optimized insulin injections remain the mainstay life-sustaining therapy for patients with T1DM (Type I DM) in 2006; however, a small subset of patients with T1DM (approx. 10%) are exquisitely sensitive to insulin and lack counter-regulatory measures, putting them at higher risk of neuroglycopenia. One alternative strategy to injected insulin therapy is pancreatic islet transplantation. Islet transplantation came of age when Paul E. Lacy successfully reversed chemical diabetes in rodent models in 1972. In a landmark study published in 2000, Shapiro et al. [A. M. Shapiro, J. R. Lakey, E. A. Ryan, G. S. Korbutt, E. Toth, G. L. Warnock, N. M. Kneteman and R. V. Rajotte (2000) N. Engl. J. Med. 343, 230–238] reported seven consecutive patients treated with islet transplants under the Edmonton protocol, all of whom maintained insulin independence out to 1 year. Substantial progress has occurred in aspects of pancreas procurement, transportation (using the oxygenated two-layer method) and in islet isolation (with controlled enzymatic perfusion and subsequent digestion in the Ricordi chamber). Clinical protocols to optimize islet survival and function post-transplantation improved dramatically with the introduction of the Edmonton protocol, but it is clear that this approach still has potential limitations. Newer pharmacotherapies and interventions designed to promote islet survival, prevent apoptosis, to promote islet growth and to protect islets in the long run from immunological injury are rapidly approaching clinical trials, and it seems likely that clinical outcomes of islet transplantation will continue to improve at the current exponential pace.
Rozprawy doktorskie na temat "Apoptosis Immunological aspects"
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Dorstyn, Loretta Esterina. "The identification and characterisation of two novel Drosophila caspases, DRONC and DECAY." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phd718.pdf.
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Includes a list of publications co-authored by the author during the preparation of this thesis. Thesis amendments in back leaf. Includes bibliographical references (leaves 123-168). The studies described concentrate on the cloning and characterisation of the two Drosophila caspases, DRONC and DECAY
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Cheung, Ka-wa Benny, and 張嘉華. "Mechanism of Bacillus Calmette Guerin-induced immune response." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29488989.
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Marshall, Aiden Christopher James 1976. "The role of Fas and TNFα in experimental autoimmune gastritis". Monash University, Dept. of Pathology and Immunology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9413.
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Lacey, Derek. "NFκB independent pathway activation of rheumatoid arthritis FLS by macrophage migration inhibitory factor (MIF)". Monash University, Faculty of Medicine, 2003. http://arrow.monash.edu.au/hdl/1959.1/9457.
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Doumont, Gilles. "Identification et caractérisation de nouveaux médiateurs de l'activité biologique de la protéine suppresseur de tumeur p53." Doctoral thesis, Universite Libre de Bruxelles, 2005. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211022.
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Le suppresseur de tumeur p53 permet à la cellule de se défendre contre différentes formes de stress. Il joue un rôle de barrière s'opposant à la tumorigenèse: en effet la perte de p53 chez la souris prédispose grandement ces animaux à développer des tumeurs; de même le locus p53 est inactivé dans près de 50% des tumeurs humaines.<p>p53 constitue un facteur de transcription qui se lie à des séquences particulières de l'ADN et active l'expression des gènes adjacents. L'expression orchestrée de ces gènes conduit, directement ou indirectement et suivant le contexte cellulaire, soit à la mort de la cellule soit à l'inhibition de la division cellulaire.<p>Les mécanismes moléculaires médiant ces deux activités biologiques essentielles de p53, de même que les mécanismes influençant le choix de la réponse cellulaire, sont encore mal compris. L'importance de p53 dans ce choix reste également à démontrer.<p>Afin de contribuer à la compréhension de ces mécanismes, le modèle murin déficient pour Mdm4, un régulateur négatif de l'activité de p53, a été choisi. L'inactivation de Mdm4 chez la souris conduit en effet à l'activation ectopique de p53 in vivo et l'induction de deux types de réponse: apoptose dans le neuroépithélium et arrêt de la prolifération cellulaire dans les tissus non neuronaux. Le profil d'expression des gènes dans les tissus neuronaux et non neuronaux a donc été comparé entre embryons de souris sauvage et mdm4-/- par la technique d'hybridation de biopuces à ADN. Les résultats obtenus suggèrent que le type de réponse dépend du type cellulaire et non de p53 lui-même. En effet les profils d'expression des gènes dans les tissus neuronaux (conditions d'apoptose) et non neuronaux (conditions d'arrêt de la prolifération cellulaire) chez l'embryon de souris mdm4-/- sont comparables.<p><p>Nous nous sommes ensuite particulièrement intéressés à deux nouveaux gènes dont l'expression est augmentée dans les embryons mdm4-/-. Dans un premier temps, leur induction transcriptionnelle chez l'embryon de souris mdm4-/- a été confirmée par différentes techniques et il a été vérifié qu'ils constituaient tous deux des cibles directes de p53 induites suite à un stress génotoxique.<p>Le premier gène code Dapk1, une protéine suppresseur de tumeur pro-apoptotique présentant une activité de type sérine/thréonine kinase. Ce travail a permis d'établir que Dapk1 participait à une boucle de rétroaction du contrôle de l'activité de p53.<p>Le deuxième gène identifié code la protéine Ptprv, un récepteur transmembranaire présentant une activité de type tyrosine phosphatase. En vue d'étudier la signification physiologique de l'induction transcriptionnelle de ptprv suite à l'activation de p53, des expériences effectuées à partir de matériel biologique issu de souris déficientes pour Ptprv ont été réalisées. Ces expériences confirment le rôle essentiel de Ptprv comme médiateur de l'arrêt du cycle cellulaire en phase G1 induit par p53 suite à un stress génotoxique, à la fois in vitro et in vivo. Par contre, Ptprv ne semble pas influencer l'apoptose induite suite à l'activation de p53. Ce travail a également permis d'établir le rôle essentiel de Ptprv dans la suppression de tumeurs induites chez la souris par activation constitutive de l'oncogène Ras.<p><br>Doctorat en sciences, Spécialisation biologie moléculaire<br>info:eu-repo/semantics/nonPublished
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Govender, Sumentheran Nadarajan. "The effects of high intensity exercise on lymphocyte DNA and antioxidant status in trained athletes." Thesis, 1998. http://hdl.handle.net/10413/7648.
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Apoptosis (programmed cell death) and exercise immunology have been the focus of research for the past five years. Trained athletes are particularly susceptible to a wide variety of viral and bacterial infections and this has been related to oxidative damage which is a mediator of apoptosis. Apoptosis, a normal physiological mechanism has also been implicated in the pathogenesis of a wide-variety of diseases. To date, the link between apoptosis and exercise has not been shown by established methods or ultrastructurally. The objective of the study was t.o determine the effects of a single bout of high intensity exercise on lymphocyte DNA and antioxidant status in trained athletes. The study was carried out in two phases.
In the first phase, 11 trained athletes were subjected to a treadmill run to exhaustion using a ramp protocol to determine their maximum oxygen uptake (V02 max). Fifteen millimetres of blood was collected before exercise, immediately after exercise, 24 hours and 48 hours after exercise. Whole blood (4 ul) was used in the determination of DNA damage in lymphocytes using the single cell gel electrophoresis (SCGE) assay. The
remaining blood was centrifuged and used for the following: Vitamin C concentration was determined by the 2,4 dinitrophenylhydrazine method, vitamin E concentration was determined by the High Pressure Liquid
Chromatography (HPLC) method and lipid peroxides were determined by the measurement ofhydroperoxides.
In the second phase, 3 trained athletes who had participated in phase 1, were subjected to a V02 max. test. Blood samples (10 ml) were collected before and immediately after exercise, 24 hours and 48 hours later.
Lymphocytes were isolated using Histopaque 1077. An in situ cell death detection kit, Fluorescein was used for the detection and quantification of apoptosis in lymphocytes at a single cell level, based on labelling of DNA strand breaks. Analysis was carried out using flow cytometry. Lymphocytes were also prepared for Transmission Electron Microscopy (TEM) using conventional techniques.
The results showed that immediately after exercise there was a non-significant decrease in vitamin C concentrations (p=o, 16), and a non-significant increase in vitamin E (p=0,82) and lipid peroxide concentrations (p=0,21). There was no significant difference in all 3 levels over the 48 hour period, when compared to the pre-exercise values. The SCGE assay revealed that the immediate post exercise samples showed DNA damage in lymphocytes of all subjects as evidenced by fluorescent strands of DNA outside the cell while DNA damage was observed in only one subsequent sample. In the pre-exercise samples, DNA was visualised as a central core, whereas in all samples taken after exercise, DNA was located at the periphery or confined to one pole of the cell. The pattern of DNA distribution seen in the SCGE assay over the 48 hour period were characteristic features of apoptosis. Flow cytometric analysis showed an increase in apoptosis in lymphocytes immediately after exercise with a further increase after 24 hours. After 48 hours the numbers decreased to control levels. TEM showed that majority of cells were normal before exercise while other lymphocytes were smaller with indented nuclei. Immediately after exercise the lymphocytes displayed features of indented nuclei and microsegregation, cell shrinkage, swelling of the endoplasmic reticulum, mitochondria and Golgi. These changes persisted after 24 hours but were not observed after 48 hours when most of the cells showed normal morphology. The ultrastructural changes observed were also characteristic features of apoptosis.
These results suggest that high intensity exercise may cause an increase in apoptosis as evidenced by DNA damage in the SCGE assay and fully supported by the results achieved during flow cytometry and by the
ultrastructural changes observed.<br>Thesis (M.Med.Sc.)-University of Natal, Durban, 1998.
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Lewis, David. "Soypeptide lunasin in cytokine immunotherapy for lymphoma." Thesis, 2014. http://hdl.handle.net/1805/4845.
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Indiana University-Purdue University Indianapolis (IUPUI)<br>Immunostimulatory cytokines can enhance anti-tumor immunity and are part of the therapeutic armamentarium for cancer treatment. We previously reported that chemotherapy-treated lymphoma patients acquire a deficiency of Signal Transducer and Activator of Transcription 4 (STAT4), which results in defective IFNy production during clinical immunotherapy. With the goal of further improvement in cytokine-based immunotherapy, we examined the effects of a soybean peptide called lunasin that exhibits immunostimulatory effects on natural killer cells (NKCs). Peripheral blood mononucleated cells (PBMCs) from healthy donors and chemotherapy-treated lymphoma patients were stimulated with or without lunasin in the presence of IL-12 or IL-2. NK activation was evaluated, and its tumoricidal activity was assessed using in vitro and in vivo tumor models. Chromatin immunoprecipitation (ChIP) assay was performed to evaluate the histone modification of gene loci that are regulated by lunasin and cytokine. Adding lunasin to IL-12- or IL-2-cultuted NK cells demonstrated synergistic effects in the induction of IFNG and genes involved in cytotoxicity. The combination of lunasin and cytokines (IL-12 plus IL-2) was capable of restoring IFNy production by NK cells from post-transplant lymphoma patients. In addition, NK cells stimulated with lunasin plus cytokines have higher tumoricidal activity than those stimulated with cytokines alone using in vitro tumor models. The underlying mechanism responsible for the effects of lunasin on NK cells is likely due to epigenetic modulation at target gene loci. Lunasin represents a different class of immune modulating agent that may augment the therapeutic responses mediated by cytokine-based immunotherapy.
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Wang, Ting. "Transfer of intracellular HIV Nef to endothelium causes endothelial dysfunction." Thesis, 2014. http://hdl.handle.net/1805/5584.
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Indiana University-Purdue University Indianapolis (IUPUI)<br>With effective antiretroviral therapy (ART), cardiovascular diseases (CVD), are emerging as a major cause of morbidity and death in the aging population with HIV infection. Although this increase in CVD could be partially explained by the toxic effects of combined anti-retroviral therapy (ART), more recently, HIV infection has emerged as an independent risk factor for CVD. However, it is unclear how HIV can contribute to CVD in patients on ART, when viral titers are low or non-detectable. Here, we provide several lines of evidence that HIV-Nef, produced in infected cells even when virus production is halted by ART, can lead to endothelial activation and dysfunction, and thus may be involved in CVD. We demonstrate that HIV-infected T cell-induced endothelial cell activation requires direct contact as well as functional HIV-Nef. Nef protein from either HIV-infected or Nef-transfected T cells rapidly transfers to endothelial cells while inducing nanotube-like conduits connecting T cells to endothelial cells. This transfer or transfection of endothelial cells results in endothelial apoptosis, ROS generation and release of monocyte attractant protein-1 (MCP-1). A Nef SH3 binding site mutant abolishes Nef-induced apoptosis and ROS formation and reduces MCP-1 production in endothelial cells, suggesting that the Nef SH3 binding site is critical for Nef effects on endothelial cells. Nef induces apoptosis of endothelial cells through both NADPH oxidase- and ROS-dependent mechanisms, while Nef-induced MCP-1 production is NF-kB dependent. Importantly, Nef can be found in CD4 positive and bystander circulating blood cells in patients receiving virally suppressive ART, and in the endothelium of chimeric SIV-infected macaques. Together, these data indicate that Nef could exert pro-atherogenic effects on the endothelium even when HIV infection is controlled and that inhibition of Nef-associated pathways may be promising new therapeutic targets for reducing the risk for cardiovascular disease in the HIV-infected population.
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Sally, Benjamin Andrew. "Failure to process chromatin on apoptotic microparticles in the absence of deoxyribonuclease 1 like 3 drives the development of systemic lupus erythematosus." Thesis, 2017. https://doi.org/10.7916/D8XG9WSQ.
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Systemic lupus erythematosus is an autoinflammatory disorder driven by the development of autoantibodies to self-nucleic acids, in particular to DNA and to chromatin. Loss-of-function mutations of the secreted deoxyribonuclease DNASE1L3 have been implicated in the development of aggressive familial lupus. In addition, recent genome-wide association studies have linked a hypomorphic variant of DNASE1L3 to sporadic lupus. Studies in the lab determined that Dnase1l3-deficient mice develop rapid autoantibody responses against dsDNA and chromatin, and at older ages this leads to a lupus-like inflammatory disease. These disease manifestations were completely independent of the intracellular DNA sensor STING, which has been implicated in other examples of self-DNA driven autoinflammatory diseases. My project focused on developing assays to track the activity of DNASE1L3, as well as identifying the endogenous source of self-DNA normally processed by DNASE1L3. Using mouse models that allow the depletion of specific cell populations, we found that circulating DNASE1L3 is produced by hematopoietic cells, in particular by CD11c+ dendritic cells and by tissue macrophages. Taking into account the unique properties of DNASE1L3, we discovered that this enzyme is uniquely able to digest chromatin contained within and on the surface of apoptotic microparticles. Loss of DNASE1L3 activity in circulation results in elevated levels of DNA in plasma, in particular within microparticles. Microparticles are extensively bound by anti-chromatin autoantibodies isolated from both murine models of lupus as well as prototypical human clones. In addition, Dnase1l3-deficient mice have high levels of circulating IgG that bind to microparticles from young ages, and these titers increased as disease progressed in aged animals. Pretreatment of microparticles with DNASE1L3 largely abrogated this binding, demonstrating that DNASE1L3 directly reduces the immunogenicity of microparticles. We also studied two human patients with null mutations in DNASE1L3, and observed increased DNA circulating in plasma and, in particular, in their microparticles, demonstrating a conserved role for DNASE1L3 in mice and humans. Finally, we obtained plasma samples from a cohort of patients with sporadic SLE, and found that roughly 80% had circulating IgG that avidly bound microparticles. Roughly half of this group failed to bind to microparticles that had been pretreated with DNASE1L3, and this DNASE1L3-sensitive group also presented with lower levels of DNASE1L3 activity. We conclude that extracellular chromatin associated with microparticles acts as a potential self-antigen capable of causing loss of tolerance to self-DNA and inflammatory disease in both mice and humans. The secretion of a DNA-processing enzyme thus represents a novel, conserved tolerogenic mechanism by which dendritic cells restrict autoimmunity.
Książki na temat "Apoptosis Immunological aspects"
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(Editor), J. Tschopp, ed. Pathways for Cytolysis. Springer-Verlag, 1995.
Znajdź pełny tekst źródłaCzęści książek na temat "Apoptosis Immunological aspects"
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Parcells, Mark S., and Shane C. Burgess. "Immunological aspects of Marek’s disease virus (MDV)-induced lymphoma progression." In Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response, 169–91. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7_11.
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