Academic literature on the topic 'Systemic Auto-Immune Disease'
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Journal articles on the topic "Systemic Auto-Immune Disease"
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Naha, K., S. Thakare, G. Vivek, and M. Prabhu. "Adenocarcinoma of lung masquerading as systemic auto-immune disease." Case Reports 2012, jun13 1 (June 14, 2012): bcr0220125822. http://dx.doi.org/10.1136/bcr.02.2012.5822.
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Leslie, R. D. G., and M. Hawa. "Twin Studies in Auto-immune Disease." Acta geneticae medicae et gemellologiae: twin research 43, no. 1-2 (April 1994): 71–81. http://dx.doi.org/10.1017/s000156600000297x.
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AbstractImmune-mediated diseases affect up to 5% of the population and are a major cause of morbidity and mortality. These diseases can be organ specific, such as insulin-dependent diabetes (IDDM) and non-organ specific, such as Rheumatoid Arthritis (RA). Identical and non-identical twins have been used to establish whether these diseases are determined by genetic or environmental factors. The results of these studies have been collated in a new section of the Mendel Institute in Rome.Diseases included in these studies included IDDM, RA, Systemic Lupus Erythematosus (SLE), Multiple Sclerosis (MS) and Myasthenia. Striking differences in concordance rates between identical and non-identical twins in all these studies suggest that genetic factors are important in causing these diseases. All the diseases are known to be associated with HLA genes on chromosome 6 which may account for some or all of the genetic susceptibility. However, in the majority of pairs the affected twin has an unaffected co-twin. These observations suggest that non-genetically determined factors, probably environmental factors and not somatic mutations, are critical. The study of unaffected co-twins, who are at high disease-risk, has allowed the identification of changes which precede and predict the clinical disease. The immune-mediated destruction in many of these diseases is probably caused by T-lymphocytes. Twin studies have shown the importance of genetic factors in determining T-cell responses. Identical twins should, therefore, provide the perfect test bed to assess the role of T-cells in immune-mediated diseases.
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Chen, Yunying, Fredrik Wermeling, Sven Petersen, Ylva Kaiser, and Mikael Karlsson. "Memory to self-antigens in Systemic Lupus Erythematosus (P4020)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 42.11. http://dx.doi.org/10.4049/jimmunol.190.supp.42.11.
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Abstract Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease associated with auto-IgG antibodies, which are produced due to defective clearance of apoptotic cells (AC) and loss of tolerance to self-antigens. SLE follows flare and remission courses; disease symptoms can come rapidly and unpredictably, suggesting the presence of immune memory to self-antigens in patients. However, experimental evidence and molecular mechanisms behind this are not known. We set up a mouse model by injecting normal mice with syngenic AC weekly for 4 weeks that breaks tolerance and induces auto-IgG production. One month later the serum auto-IgG drops to pre-immune level, these mice can rapidly respond to a single AC injection and produce increased auto-IgGs. This memory-like response is transferable into naïve mice. Serum level of auto-IgG subclass IgG2, but not IgG1, is dramatically increased in the memory response compared to that in the primary response, which contribute to pathogenic effects. The memory auto-IgGs are produced via both germinal center and plasmablast pathways. Spectratyping shows that B-cell repertoire is more skewed in memory response than that in pre-immune and primary response. These observations demonstrate an inducible immune memory to self-antigen in normal mice and establish a model for study of SLE flare-like response in mice. In addition, this study suggests that the formation of immune memory to self-antigens contributes to the disease relapse in SLE patients.
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J.P, Pramod. "Decoding the Mysteries of Auto-Immune Disorders." International Journal for Research in Applied Science and Engineering Technology 12, no. 8 (August 31, 2024): 1366–71. http://dx.doi.org/10.22214/ijraset.2024.64123.
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An autoimmune disease (AI) happens when the immune system doesn’t recognise its cells. This leads to a problem with how it reacts to these cells. Some of these diseases can be due to your genes, the environment, or even certain infections. They can affect specific organs or the whole body. Examples of autoimmune diseases are insulin-dependent diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, scleroderma, thyroiditis, and multiple sclerosis. But wait—there's more! Other conditions like arteriosclerosis, inflammatory bowel disease, schizophrenia, & some types of infertility also fall into this category. Around 3% of people in North America & Europe have autoimmune disorders. About three out of four people affected are women. How our immune system works and maintains tolerance is a wonder. The present paper aims to explore autoimmune diseases and what causes the immune system to react in a specific way
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Hsu, Eugene, and Manishi Desai. "Glaucoma and Systemic Disease." Life 13, no. 4 (April 15, 2023): 1018. http://dx.doi.org/10.3390/life13041018.
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Glaucoma is the leading cause of irreversible blindness in the world. Due to its potential to cause permanent vision loss, it is important to understand how systemic conditions and their respective treatments can be associated with or increase the risk for developing glaucoma. In this review, we examined the literature for up-to-date discussions and provided commentary on glaucoma, its pathophysiology, and associated risk factors. We discuss systemic diseases and the impact, risk, and mechanism for developing glaucoma, including pharmacologically induced glaucoma; inflammatory and auto-immune conditions; infectious, dermatologic, cardiovascular, pulmonary, renal, urologic, neurologic, psychiatric and systemic malignancies: intraocular tumors; as well as pediatric, and genetic conditions. The goal of our discussion of systemic conditions including their commonality, mechanisms, treatments, and associations with developing glaucoma is to emphasize the importance of ocular examinations and follow-up with the multidisciplinary teams involved in the care of each patient to prevent unnecessary vision-loss.
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Kamiya, Koji, Megumi Kishimoto, Junichi Sugai, Mayumi Komine, and Mamitaro Ohtsuki. "Risk Factors for the Development of Psoriasis." International Journal of Molecular Sciences 20, no. 18 (September 5, 2019): 4347. http://dx.doi.org/10.3390/ijms20184347.
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Psoriasis is an immune-mediated genetic skin disease. The underlying pathomechanisms involve complex interaction between the innate and adaptive immune system. T cells interact with dendritic cells, macrophages, and keratinocytes, which can be mediated by their secreted cytokines. In the past decade, biologics targeting tumor necrosis factor-α, interleukin (IL)-23, and IL-17 have been developed and approved for the treatment of psoriasis. These biologics have dramatically changed the treatment and management of psoriasis. In contrast, various triggering factors can elicit the disease in genetically predisposed individuals. Recent studies suggest that the exacerbation of psoriasis can lead to systemic inflammation and cardiovascular comorbidity. In addition, psoriasis may be associated with other auto-inflammatory and auto-immune diseases. In this review, we summarize the risk factors, which can be divided into two groups (namely, extrinsic and intrinsic risk factors), responsible for the onset and exacerbation of psoriasis in order to facilitate its prevention.
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Bird, Anna Kathleen, Javier Rangel-Moreno, Nida Meednu, Jennifer Hossler, and Jennifer Anolik. "Neutrophils modulate the progression of B cell auto-reactivity in systemic lupus erythematosus." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 117.3. http://dx.doi.org/10.4049/jimmunol.196.supp.117.3.
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Abstract The central feature of systemic lupus erythematosus (SLE) pathogenesis is loss of immunologic self-tolerance. Here, we address a current controversy regarding whether neutrophils influence the development of B cell auto-reactivity SLE. While both human and murine lupus neutrophils produce factors known to fuel adaptive immune dysregulation, including type I interferon, B cell survival factors, and extracellular traps (a putative source of self-antigen), some studies have contended that neutrophils in peripheral lymphoid organs (PLO) suppress B cell activation and differentiation. In order to ask whether neutrophils exert regulatory or deleterious effects on loss of B cell self-tolerance and immune activation, we compare changes in SLE progression following neutrophil depletion in the NZB/W lupus model, either during or after establishment of disease. Following depletion early in disease, we observe pronounced acceleration of proteinuria, anti-dsDNA titers, and germinal center formation. However, neutrophil depletion after onset of overt disease pathology (including proteinuria) does not strongly alter SLE progression, implicating neutrophils as playing a protective role only apparent during disease onset. To elucidate the specific mechanisms underlying neutrophil effects on B cell auto-reactivity, we examine the cytokine profile of neutrophils in direct proximity to B cells in PLO during several stages of disease. With progression of disease, we observe an influx of interferon-alpha-producing neutrophils in direct proximity to B cells in PLO. These data delineate a shifting balance of both regulatory and activating roles for neutrophils in auto-reactive B cell activation/proliferation during SLE progression.
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Hossain, Md Ismail, Shah Md Sarwer Jahan, Md Ashraful Haque, ABM Mobasher Alam, Mainuddin Ahmed, and Md Zakir Hossain. "Systemic lupus erythematosus in male: two case reports." Bangladesh Journal of Medicine 24, no. 2 (August 27, 2014): 82–85. http://dx.doi.org/10.3329/bjmed.v24i2.20222.
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Systemic lupus erythematosus (SLE) is the most common multisystem connective tissue disease. Around 90% of affected individuals are women, with peak onset in the second and third decades. Tissues of all system are damaged by pathogenic auto-antibodies and immune complexes. We report here two cases of SLE in male patient, presented with typical features of SLE. Though the disease is rare in male, but such type of manifestations should be investigated properly to exclude SLE. DOI: http://dx.doi.org/10.3329/bjmed.v24i2.20222 Bangladesh J Medicine 2013; 24 : 82-85
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Yang, Yening. "The comparison between different therapies of Systemic Lupus Erythematosus." Theoretical and Natural Science 49, no. 1 (November 15, 2024): 9–15. http://dx.doi.org/10.54254/2753-8818/49/20241257.
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Abstract. The immune system has three basic functions: defense, surveillance and homeostasis. It helps us monitoring and timely eliminate mutant cells and distinguishing between alien components to maintain self-stability. However, once it loses these abilities, it could cause the autoimmune disease. In this article, I mainly discuss about the Systemic Lupus Erythematosus (SLE), a type of autoimmune diseases which is mediated by type hypersensitivity. SLE patients suffer from chronic inflammatory responses, leading to tissue damage and organ dysfunction. Therefore, purpose of therapeutic schedule is to inhibit the overactive immune system and relieve the inflammatory response. Nowadays, there are three major therapies: Glucocorticoids (GC), immunosuppression agents and belimumab. Glucocorticoids suppresses inflammatory responses and generate anti-inflammatory factors. Immunosuppression agents can not only control SLE and raise the survival rate of long-term prognosis for SLE patients. Belimumab inhibits the survival of B cells by obstructing the interaction between soluble B cell activating factor (BAFF or BLys) and receptors on B cells. This action promotes the apoptosis of auto-reactive B cells, leading to a decrease in auto-antibodies present in the serum. With the development of biotechnology, more and more advanced treatments have emerged and brings new hope to SLE patients.
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Hudspeth, Kelly L., Wang Shu, Jingya Wang, Saifur Rahman, Michael A. Smith, Kerry Anne Casey, Geoffrey L. Stephens, et al. "NK cell phenotype and proliferation in Systemic Lupus Erythematosus." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 194.5. http://dx.doi.org/10.4049/jimmunol.196.supp.194.5.
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Abstract Systemic Lupus Erythematosus (SLE) is a complex autoimmune disorder whose pathology appears to involve many immune cell types. While it is clear that autoantibody producing B cells as well as CD4+ T cell help are key contributors to disease, little is known regarding the role of innate lymphoid cells such as Natural Killer (NK) cells in the pathogenesis of SLE. We have characterized the phenotype of NK cells by multicolor flow cytometry in a large cohort of SLE patients. While the overall percentage of NK cells was similar or slightly decreased compared to healthy controls, a subset of patients displayed a high frequency of NK cells expressing the proliferation marker, Ki-67, which was not found in healthy donors. Only a moderate increase of Ki-67 was observed on other immune cell types such as total CD4+, CD8+ T cells or CD19+ B cells in the same donors. Increased NK cell proliferation was found to correlate with clinical parameters. Furthermore, proteomics analysis and auto-antibody arrays revealed significant correlations between NK cell expression of Ki-67 and specific serum protein biomarkers, as well as SLE associated auto-antibodies. These results will contribute to the understanding of the mechanistic role of NK cells in immune-mediated pathology of SLE.
Dissertations / Theses on the topic "Systemic Auto-Immune Disease"
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Depaire, Agathe. "Altérations de l’efferocytose des macrophages induits par les cellules endothéliales : analyse des mécanismes et approche thérapeutique pour corriger la vasculopathie et la fibrose au cours de la sclérodermie systémique." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0481.
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La sclérodermie systémique (ScS) est une maladie auto-immune fibrotique chronique incurable. Le concept de réparation tissulaire non résolue, menant à une fibrose persistante, a émergé sur la base d'une inflammation stérile chronique qui transforme une réponse de réparation contrôlée en fibrose pathologique. La résolution efficace de l'inflammation repose notamment sur l’élimination des cellules apoptotiques par les macrophages (Mϕ) via l’efferocytose. Récemment, mon équipe a montré le rôle de la stimulation des cellules endothéliales microvasculaires (CEMV) cutanées par l’IL-1β dans la modulation de la polarisation macrophagique vers un profil mixte M1/M2 inflammatoire, et son implication dans la fibrose cutanée sclérodermique. Une analyse transcriptomique à partir de biopsies cutanées, a mis en évidence une signature de gènes associés à l’efferocytose diminuée chez les patients ScS par rapport aux contrôles. Ce travail visait, par des analyses in vitro à partir de cellules purifiées de la peau de patients ScS ou de sujets sains, à déterminer si les CEMV et l'IL-1β contribuent à l'altération de l’efferocytose au cours de la ScS, et à évaluer les conséquences sur l'activation des fibroblastes et la transition endothélio-mésenchymateuse (EndoMT). Pour cela, les macrophages dérivés de monocytes ont été générés en présence de surnageant de CEMV activées (CEMVIL-1β-Mϕ) ou non (CEMV-Mϕ) par l’IL-1β.Nos résultats mettent en évidence une diminution significative de la phagocytose de Jurkat apoptotiques (apoJK) par les CEMVIL-1β-Mϕ associée à une diminution de l’expression de certains récepteurs directs ou indirects impliqués dans l’efferocytose. D’autre part, l'ajout d'IL-1β pendant la différenciation des MDM0 (contrôle positif de phagocytose) n'a pas altéré leur profil efferocytique global suggérant que l'effet inhibiteur de l'IL-1β ne se manifeste qu'en présence du sécrétome endothélial. Nous avons ensuite étudié les effets du sécrétome macrophagique post-efferocytose sur l’activation fibroblastique et l’EndoMT. Les CEMVIL-1β-Mϕ favorisent le phénotype pro-remodelant et inflammatoire des fibroblastes, effet qui n’est pas limité par la présence de TGF-β et qui est d’autant plus prononcé dans les conditions efferocytiques sclérodermiques. Sur le plan de l’EndoMT nos résultats indiquent que les CEMVIL-1β-Mϕ semblent initier l’EndoMT uniquement dans les conditions ScS en augmentant l’expression de l’α-SMA et de la fibronectine des CEMV. En revanche, les CEMV-Mϕ ont favorisé un phénotype profibrotique des fibroblastes uniquement en présence du surnageant efferocytique combiné au TGF-β et n’induisent pas d’initiation de l’EndoMT.Dans le cadre de cette thèse CIFRE, nous avons exploré le potentiel anti-inflammatoire et pro-résolutif du Résolvix©, candidat médicament développé par la société MIP, basé sur un sécrétome de Mϕ de sujets sains ayant réalisé une efferocytose. Nos résultats montrent qu’en présence de Résolvix©, les fibroblastes sclérodermiques des patients voient diminuer leur profil fibrotique au profit d’un profil remodelant et sécréteur de CCL2. Ce dernier permet également de reverser un profil myofibroblastique déjà établi, tout en favorisant la production de CCL2. Nos données montrent que l’efferocytose joue un rôle variable selon l’état d’activation des CEMV, reflétant potentiellement un rôle séquentiel dans la ScS dans la mesure où l'IL-1β est augmenté dans la peau des patients à des stades précoces, alors que le TGF-β semblent jouer un rôle à des stades tardifs.Ces résultats suggèrent que la restauration d’une efferocytose efficace pourrait limiter l’inflammation et la fibrose au cours de la ScS. Le Résolvix©, pourrait restaurer un environnement tissulaire limitant la fibrose tout en favorisant le recrutement de nouveaux macrophages aux capacités d’efferocytose restaurés chez les patients sclérodermiques ayant des formes tardives avec une fibrose bien établieSystemic sclerosis (SSc) is an incurable chronic fibrotic autoimmune disease. The concept of unresolved tissue repair, leading to persistent fibrosis, has emerged based on chronic sterile inflammation, which transforms a controlled repair response into pathological fibrosis. Effective inflammation resolution relies on macrophages' (Mϕ) efferocytosis, the clearance of apoptotic cells. Recently, my team demonstrated the role of IL-1β-stimulated cutaneous microvascular endothelial cells (MVEC) in modulating macrophage polarization towards a mixed M1/M2 inflammatory profile, implicating this process in cutaneous sclerodermic fibrosis. Transcriptomic analysis from skin biopsies highlighted a gene signature associated with reduced efferocytosis in SSc patients compared to controls. This study aimed, through in vitro analyses of purified cells from SSc patients' or healthy donors' skin, to determine whether MVEC and IL-1β contribute to efferocytosis alteration during SSc and evaluate the consequences on fibroblast activation and endothelial-mesenchymal transition (EndoMT). Monocyte-derived macrophages were generated in the presence of supernatant from MVEC either activated (MVECIL-1β-Mϕ) or not (MVEC-Mϕ) by IL-1β.Our results show a significant reduction in the phagocytosis of apoptotic Jurkat cells (apoJK) by MVECIL-1β-Mϕ, associated with decreased expression of certain direct or indirect receptors involved in efferocytosis. Conversely, adding IL-1β during MDM0 (positive control for phagocytosis) differentiation did not alter their overall efferocytic profile, suggesting that IL-1β's inhibitory effect manifests only in the presence of the endothelial secretome. We then studied the effects of post-efferocytosis macrophage secretome on fibroblast activation and EndoMT. MVECIL-1β-Mϕ promoted a pro-remodeling and inflammatory fibroblast phenotype, unaffected by TGF-β, and more pronounced in sclerodermic efferocytic conditions. Regarding EndoMT, our results indicate that MVECIL-1β-Mϕ appears to initiate EndoMT only in SSc conditions, increasing α-SMA and fibronectin expression in MVEC. However, MVEC-Mϕ promoted a pro-fibrotic fibroblast phenotype only in the presence of efferocytic supernatant combined with TGF-β and did not induce EMT initiation.As part of this CIFRE thesis, we explored the anti-inflammatory and pro-resolutive potential of Résolvix, a drug candidate developed by MIP, based on the secretome of Mϕ from healthy subjects who had undergone efferocytosis. Our results show that in the presence of Résolvix©, sclerodermic fibroblasts from patients exhibit a decrease in their fibrotic profile in favor of a remodeling and CCL2-secreting profile. This also allows for the reversal of an already established myofibroblastic profile while promoting CCL2 production. Our data indicate that efferocytosis plays a variable role depending on the activation state of the vascular endothelial cells, potentially reflecting a sequential role in systemic sclerosis, as IL-1β is elevated in the skin of patients at early stages, while TGF-β seems to play a role at later stages.These results suggest that restoring effective efferocytosis could limit inflammation and fibrosis during SSc. Résolvix© could restore a tissue environment that limits fibrosis while promoting the recruitment of new macrophages with restored efferocytosis capabilities in sclerodermic patients with late-stage forms and established fibrosis
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Nguyen, Vinh. "Développement d’un nouveau modèle murin expérimental de sclérodermie." Thèse, 2016. http://hdl.handle.net/1866/13888.
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La sclérodermie (SSc) est une maladie rare affectant les personnes génétiquement prédisposées d’une réponse immunitaire défectueuse. Malgré les derniers avancements et développements dans le domaine, l’étiologie et la pathogénèse de la maladie demeurent peu comprises. Par ailleurs, il y a un ralentissement dans la compréhension de cette maladie à cause du manque de modèle animal représentatif de la SSc humaine. Malgré plusieurs lacunes, les souris traitées avec la bléomycine ou portant des modifications génétiques (TSK-1) sont très utilisées dans les études précliniques de la SSc mais elles ne présentent pas toutes les caractéristiques de cette maladie. Pour contribuer à la recherche sur la SSc, la stagiaire postdoctorale Dre Heena Mehta a développé dans le laboratoire du Dre Sarfati en collaboration avec le Dr Senécal, un modèle de souris expérimental induit par l’immunisation de cellules dendritiques (DCs) chargées de peptides de la protéine topoisomérase I (TOPOIA et TOPOIB). Dans le but de caractériser ce modèle murin et d’établir un profil immunitaire, j’ai concentré mes analyses principalement sur les caractéristiques de la SSc telles que la fibrose, l’inflammation, l’hyper-γ-globulinémie polyclonale, la vasculopathie ainsi que de l’expression de cytokines. Brièvement, l’immunisation de souris avec les DCs chargées avec la topoisomérase I (TOPOI) a induit l’inflammation pulmonaire et cutanée, en plus de la fibrose sous forme diffuse (dcSSc). Les souris présentaient également des symptômes de la vasculopathie ainsi que des taux élevés d’anticorps polyclonaux. Les résultats démontraient que les peptides TOPOIA étaient efficaces dans l’induction de la fibrose et de la réponse inflammatoire alors que les peptides TOPOIB étaient surtout impliqués dans la fibrose cutanée. En plus de nos résultats, les observations préliminaires sur le profil de cytokines tissulaires suggéraient que ce modèle pourrait remplacer ou complémenter les autres modèles animaux de SSc.Systemic sclerosis (SSc) is a rare disease of unknown etiology that affects people that have a genetic predisposition to autoimmunity. Despite the latest advancement and development in the field, the mechanisms underlying disease development remain poorly understood. The lack of animal model that encompasses the cardinal features of human systemic sclerosis is a major cause of the slowdown in the understanding of this disease. In fact, some mouse models such as the bleomycin induced-SSc and TSK-1 mouse are widely used in preclinical studies of scleroderma. However, these models have several shortcomings since these mice do not display all the cardinal features of the disease found in humans. To contribute to the research of SSc, postdoctoral fellow Dre Heena Mehta has developed in Dre Sarfati’s laboratory in collaboration with Dr Senécal, an experimental murine model of SSc induced by dendritic cells loaded with topoisomerase I peptide. In order to characterise the model and establish an immune profile of our experimental mice, my analysis focused mainly on the cardinal features of scleroderma such as fibrosis, inflammation and polyclonal hyper-γ-globulinemia, vasculopathy and cytokines gene expression. Hence, immunization with dendritic cells loaded topoisomerase I peptides (TOPOIA and TOPOIB) induced pulmonary and dermal inflammation together with diffuse form of fibrosis. The mice also showed symptoms of vasculopathy and high levels of polyclonal antibodies. These results showed that TOPOIA peptides are effective in inducing fibrosis and inflammatory response while TOPOIB peptides are involved in skin fibrosis. Together with the results, the preliminary data on cytokine profile in tissue suggested that our mouse model could possibly replace/complement other current animal models of scleroderma.
Books on the topic "Systemic Auto-Immune Disease"
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Berden, Jo H. M., and Jack F. M. Wetzels. Immunological investigation of the patient with renal disease. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0017.
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Laboratory techniques (electrophoresis, indirect immunofluorescence, ELISA, and immunoblotting) required for immunological investigation of the patient with renal disease are described. Renal disease-related aspects of immunoglobulins (immunoglobulin A, paraproteins, cryoglobulins), complement, antinuclear antibodies, anti-C1q antibodies, antineutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies, antipodocyte antibodies, antiphospholipid antibodies, and antimicrobial responses (streptococci, hepatitis C, hepatitis B) are reviewed. Laboratory assays which evaluate the immune response, in particular the identification of (auto)-antibodies are valuable tools in establishing a diagnosis and/or monitoring of the activity of the disease. Guidelines are given for immunological studies in patients with specific renal syndromes including nephrotic syndrome, rapidly progressive glomerulonephritis, systemic lupus erythematosus, and thrombotic microangiopathy.
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Multi-systemic auto-immune diseases: An integrated approach : dermatological and internal aspects. Amsterdam: Elsevier, 1995.
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Kater, Louis, and Harold Baart De LA Faille. Multi-Systemic Auto-Immune Diseases: An Integrated Approach : Dermatological and Internal Aspects. Elsevier Science Pub Co, 1999.
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Klenerman, Paul. The Immune System: A Very Short Introduction. Oxford University Press, 2017. http://dx.doi.org/10.1093/actrade/9780198753902.001.0001.
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The Immune System: A Very Short Introduction describes the immune system and how it works in health and disease. It focuses on the human immune system, considering how it evolved, and the basic rules that govern its behaviour. The immune system comprises a series of organs, cells, and chemical messengers that work together as a team to provide defence against infection. These components are discussed along with the critical signals that trigger them and how they exert their protective effects, including innate and adaptive responses. The consequences of too little immunity (immunodeficiency), caused for example by HIV/AIDS, and too much, leading to auto-immune and allergic diseases, are also considered.
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Dalbeth, Nicola. Pathophysiology of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0039.
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The clinical features of gout occur in response to monosodium urate (MSU) crystals. Gout should be considered a chronic disease of MSU crystal deposition. A number of pathophysiological checkpoints are required for development of gout. First, elevated urate concentrations are required: urate overproduction and underexcretion contribute to total urate balance. Overproduction occurs due to alterations in the purine synthesis and degradation pathways. Renal underexcretion is an important cause of elevated serum urate concentrations (hyperuricaemia), and occurs through alterations in the urate transporters within the renal tubule (collectively known as the urate transportasome). Gut underexcretion (extrarenal urate underexcretion) also contributes to development of hyperuricaemia. The next checkpoint is MSU crystal formation. In some individuals with evidence of MSU crystal deposition, symptomatic gout develops. The acute inflammatory response to MSU crystals represents a self-limiting sterile acute auto-inflammatory response which is mediated by the innate immune system activation. Interleukin 1 beta is the key cytokine that contributes to the acute inflammatory response to MSU crystals. In some patients, advanced gout may occur with structural joint damage. Joint damage in gout is mediated both by direct effects of MSU crystals on joint tissue and by indirect effects of joint inflammation. In addition to their central role in pathogenesis of gout, MSU crystals have a physiological role, particularly as an adjuvant or ‘danger signal’ in immune surveillance.
Book chapters on the topic "Systemic Auto-Immune Disease"
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Greco, Raffaella, and Dominique Farge. "CART Cells and Other Cell Therapies (ie MSC, Tregs) in Autoimmune Diseases." In The EBMT Handbook, 837–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_93.
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AbstractAuto-immune diseases (AD) are heterogeneous conditions, characterized by polyclonal activation of the immune system with a defect of B or T lymphocyte selection and altered lymphocytic reactions to auto-antigens components (Burnet 1959a, b), although it is rare to identify a single antigenic epitope. The native immune system and its tissue environment play an important role to determine if exposure to a given antigen will induce an immune response or tolerance or anergy. The role of the genes coding for the major histocompatibility system molecules, but also of many other genes, is important in the regulation of the immune response, although this does not explain all the observed phenomena during loss of tolerance (Matzinger 1994; Rioux and Abbas 2005).
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Hall, Angela, Chris Scott, and Matthew Buckland. "Autoimmune skin disease." In Clinical Immunology. Oxford University Press, 2016. http://dx.doi.org/10.1093/hesc/9780199657650.003.0008.
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This chapter looks at autoimmune skin diseases such as pemphigoid and pemphigus. It notes how auto-antibodies are directed against protein at the dermal-epidermal junction in the pemphigoid, while pemphigus has auto-antibodies directed against cell junctions in the epidermis. The chapter indicates that specific auto-antibodies are associated with disruption of the skin structure leading to blistering. Biopsies or serums can demonstrate the presence of auto-antibodies as well. The chapter shows how treatment can include steroid, topic, systemic, steroid-sparing systemic immune suppression, high dose intravenous immunoglobulin, plasmapheresis in conjunction with systemic immune suppression, or monoclonal antibody therapy targeting B lymphocytes. In addition, it references other autoimmune blistering skin disorders such as dermatitis herpetiformis and toxic epidermal necrolysis.
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Monroy-Trujillo, Jose Manuel, and Duvuru Geetha. "Systemic Inflammatory Diseases and the Kidney." In Kidney Protection, edited by Vijay Lapsia, Bernard G. Jaar, and A. Ahsan Ejaz, 327–36. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190611620.003.0033.
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The kidneys are targets of systemic autoimmunity as well as pathogenic immune responses against renal auto antigens. Systemic autoimmunity against ubiquitous antigens leading to renal inflammation is seen in antineutrophil cytoplasmic antibodies (ANCA) associated vasculitis, immunoglobulin (Ig) A vasculitis, systemic lupus erythematosis, scleroderma and IgG4 disease while immune responses against specific renal antigens is seen in antiglomerular basement membrane disease. Renal involvement can be the presenting feature in these diseases and can manifest as a rise in serum creatinine or asymptomatic urinary abnormalities or can present with rapidly progressive renal failure. For the majority of systemic inflammatory disorders, renal involvement heralds a poor prognosis and warrants timely initiation of immunosuppressive therapy. This chapter will review the clinical, laboratory, and histologic features and discuss management of renal disease associated with ANCA-associated vasculitis, IgA vasculitis, antiglomerular basement membrane disease, polyarteritis nodosa, scleroderma, and IgG4 disease.
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Shimpi, Pooja, Smita Pillewan, and Vandana S. Nikam. "Diseases and Disorders Associated with Immune System." In Natural Immunomodulators: Promising Therapy for Disease Management, 41–74. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123258123010005.
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The human immune system is one of the complex systems of the body, which works against both external and internal invasion. It has two parts: the innate and the acquired immune systems. We have been born with the innate system which gives a quick response for the invading pathogen non-specifically. To deal with the typical environmental antigens, immune system adapts to changes. The acquired (or adaptive) component develops over time and produces antibodies that “remember” invaders to fight them if they return. Failure of it could be due to genetic defect (weak natural immunity), inability to adapt to the change, hyper-responsiveness, or inability to distinguish self from foreign, leading to various diseases and disorders. Various genetic defects of the immune system are at the core of Primary Immune disorders (PIDs), while overactivity is responsible for allergic diseases. Autoimmune diseases are mostly due to malfunction of the adaptive immune system, while in Systemic Auto-inflammatory Disorders (SAIDs), the innate immune system is affected. Advancements in technology and genetics have improved our understanding of the pathogenesis, diagnosis, and management of these diseases.
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Reséndiz-Mora, Albany, Alonso Tescucano, Giovanna Barrera-Aveleida, Anahi Sotelo-Rodríguez, Christian-Irene Nevárez-Lechuga, Iván Galarce-Sosa, Isabel Wong-Baeza, Isabel Baeza, and Carlos Wong-Baeza. "Anti-Non-Bilayer Phospholipid Arrangement Antibodies Trigger an Autoimmune Disease Similar to Systemic Lupus Erythematosus in Mice." In Systemic Lupus Erythematosus - Pathogenesis and Management [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106373.
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Anti-lipid antibodies are present in some infectious and autoimmune diseases, such as Systemic Lupus Erythematosus (SLE). Particularly, anti-non-bilayer phospholipid arrangement (NPA) antibodies have been detected in patients with SLE, and these antibodies trigger a disease similar to human lupus in mice. NPA are lipid associations different from the lipid bilayer of cellular membranes and, since they are transient, they are not immunogenic. However, if NPA are stabilized by drugs, they induce an immune response with the production of anti-NPA antibodies, which bind to NPA on cell membranes and generate cell lysis. As a result, intracellular antigens are exposed and trigger an immune response that generates more auto-antibodies. In this chapter, we describe the formation and stabilization of NPA, the induction of B cell responses to generate anti-NPA antibodies, and the characteristics that the disease caused by these antibodies in mice shares with human lupus.
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Vanditha, Mohan, Sonu Das, and Mathew John. "Lipid Metabolism and Associated Molecular Signaling Events in Autoimmune Disease." In Fatty Acids - Recent Advances [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105746.
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Lipid metabolism, when dysregulated paves the way to many autoimmune disease conditions. One such recently explored mechanism was that of Liver X receptor (LXR) signaling which acts as a molecular link between lipid metabolism and inflammation. LXR plays a critical role in coupling immune cell lipid homeostasis with systemic immune responses. In this chapter, we will discuss how an altered lipid metabolite environment causes inflammation signaling via LXR-mediated molecular events which could lead to autoimmune disease. In a hyperlipidemic environment, Interferon regulatory factor 3(IRF3) mediated downregulation of LXR signaling in innate immune cells leading to an inflammatory auto-immune response. Meanwhile, dendritic cell-mediated cytokine generation amidst LXR downregulation leads to the differentiation of autoreactive T cells and B cells, conferring an autoimmune response. Recent advances in the therapeutic management of autoimmune diseases target specific metabolic events as a strategy to limit inflammation and the autoimmune outcome. Novel treatment regimes in autoimmune diseases featuring lipid metabolic pathways are also discussed.
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Martínez-Jiménez, Santiago. "Introduction to Connective Tissue Disorders and Autoimmune Conditions." In Chest Imaging, 339–41. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0058.
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A variety of pathologic processes affect the connective tissues. The chapters that follow this one address some of these conditions with special emphasis on autoimmune disorders (e.g. rheumatoid arthritis, scleroderma, systemic lupus erythematosus, dermatomyositis/polymyositis, Sjögren syndrome, mixed connective tissue disease, and vasculitis), amyloidosis and eosinophilic lung disease. An autoimmune response is an immune response that targets an antigen within the host and attacks healthy body tissues. This often involves T and B lymphocytes in a response that is very similar to an allergic reaction. While the presence of an auto-antibody is often an essential component of the autoimmune response, its mere presence does not define the disease. In addition to the presence of auto-antibodies, the presence of soft tissue damage is required, thus auto-antibodies may be present in the absence of an inflammatory process. Amyloidosis is a pathologic entity with protean manifestations, often thought of as a single disease rather a group of diseases that share a similar pathophysiologic event: the deposition of proteins within the soft tissues. The term eosinophilic lung disease encompasses a wide variety of pathologic conditions that range from idiopathic diseases to systemic vasculitides and, in some cases, a response to parasitic infestation.
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Pathak, Soumya, and Dr Shambaditya Goswami. "ANTIPSORIATIC GEL FORMULATIONS: AN UPDATED WRITE UP." In Futuristic Trends in Pharmacy & Nursing Volume 3 Book 17, 150–60. Iterative International Publishers, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/v3bkpn17p5ch2.
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Topical monotherapy in patients with mild to moderate psoriasis has proved to be practically constructive along with their adjuvant role in moderate to severe psoriasis under treatment with systemic medications and phototherapy. However mild psoriasis can usually be controlled by topical therapies exclusively. Therapeutic armamentarium of topical drug delivery especially gel formulations for such debilitating auto-immune disease is ever expanding aiming at increasing patient acceptability and adherence to treatment regimen which is likely to improve ease of formulation application and its outcome based upon selection of drugs, vehicles and frequency of application. The review emphasizes on various gel formulations engaged in topical mono and/or combined therapy in treatment of psoriasis.
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Pandya, Purvi M., Ekta N. Jayswal, and Yash Shah. "Spread of Tuberculosis Among Smokers." In Mathematical Models of Infectious Diseases and Social Issues, 49–73. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-3741-1.ch003.
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Smoking tobacco has some hazardous implications on an individual's physical, physiological, and psychological health; health of the passive smokers near him or her; and on the surrounding environment. From carcinomas to auto-immune disorders, smoking has a role to play. Therefore, there arises a need to frame a systemic pathway to decipher relationship between smoking and a perilous disease such as tuberculosis. This research work focuses on how drugs or medications can affect individuals who are susceptible to tuberculosis because of smoking habits and also on individuals who have already developed symptoms of tuberculosis due to their smoking addiction. The mathematical model is formulated using non-linear ordinary differential equations, and then threshold is calculated for different equilibrium points using next generation matrix method. Stability analysis along with numerical simulations are carried out to validate the data.
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Bhowmik, Diptendu, Venu Kola, Subba Rao Chamakuri, and Chiranjib Bhattacharjee. "Rheumatoid Arthritis: Introduction." In Natural Products for the Management of Arthritic Disorders, 1–25. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050776122010003.
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Rheumatoid Arthritis elaborated as Rheumatoid Arthritis is a systemic chronic inflammatory condition that might affect numerous organs and tissues in a human body, but mainly it attacks the synovial joints. These methods result in the inflammatory synovitis (synovium) response. Factors that lead to an increase in the risk of rheumatoid arthritis are age, sex, family history, smoking, obesity, and exposure to pollutants. RA holds the ability to put a person at a higher risk of developing other medical conditions if it is not controlled timely. A syndrome named carpal tunnel is another common condition found in people suffering from rheumatoid arthritis. Trauma, infection, smoking cigarettes are some of the examples of external triggers which can trigger the reaction of the auto-immune system, which results in chronic joint inflammation and synovial hypertrophy in addition to a potential of other manifestations, which will be theorized for going on in people prone genetically. The pathological process of the disease usually results in destructing the articular cartilage as well as the joints ankylosis. Rheumatoid Arthritis could also result in diffusive lung inflammation, sclera, pleura, pericardium, as well as nodular lesions, which are also common in subcutaneous tissue. However, the causes of RA are still not known, the autoimmunity holds an important part in both the progression and chronicity. Rheumatoid Arthritis is a systemic disorder. RA can be prevented by using coldwater, living fish oil, from the herring, cod, mackerel, and salmon fish, which contains omega-3 fatty acids in high amounts, Vitamin-D supplements, and adopting the lifestyle modifications such as avoiding smokingand weight loss.
Conference papers on the topic "Systemic Auto-Immune Disease"
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Stemeier, K., J. Mertin, J. Pill, and F. Hartig. "EFFECTS OF THROMBOXANE RECEPTOR BLOCKER BM 13.505 ON THE DEVELOPMENT OF PROTEINURIA IN AUTOIMMUNE NZB/W MICE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643757.
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Female F1 hybrid of New Zealand black and white mice(NZB/W) spontaneouslydevelop an autoimmune disease characterize by afatal immune complex glomerulonephritis.Theyare considered to be a relevant model of human systemic lupus erythematosus. We observeda doubling of the concentration of TXB2 in urine at the same time when onset of proteinuria was noticed. This suggests that TXA2 synthetized by mesangial and epithelial cells of the glomeruli as well as by some inflammatory cells and platelets might be an important mediator in the pathogenesis of thi auto immune-mediated glomerular disease. Weused BM 13.505 as an long-acting TX receptor blocker for evaluating the importance of TXA2 on the development of proteinuria and compared its effects with that of the immunsuppressive agent cyclophosphamide.NZB/W mice were distributed to vehicle-treated (V-)group 20 mg/kg BM 13.505 (BM-) group and 20 mg/kgcyclophosphamide (C-) group( = 13 -14).Daily dosing by gavage was startedat the age of12 weeks. Every fourth week theurinary concentrations of proteins were measured by th biuret method and TXB2by a RIA. An increasein TXB2 was seen in the V- and BM-group, while in the C-group TXB2 was lowered. At 36 weeks of age 8of 14 animals of the V-group were proteinuria positive (>100 mg/100 ml). The study was finished at 44 weeks because more than 2/3 of the animals of the V-group haddeveloped a proteinuria. Previously four animals died and in most of other the disease was faradvanced. In the BM-group no animal had diedor showed signs of illness. However seven ofthe animals had slightly elevated protein concentrations in urine and two moderate elevated values. In the C-group no proteinuria was detected. Histological examinations of thekidneys showed a correlation in individualanimals of the V-group between the duration and extent of proteinuria and changes in the morphology of the glomeruli. In the BM-treated animals slight to moderate protein deposits were detectable, while in cyclophosphamide-treated animals glomeruli were of normal structure. This study presents someevidence that TXA2 may be an important mediator in the pathogenesis of this immune-mediated renal disease. Manifestation of this disease is delayed by the administration of thespecific TX receptor blocker BM 13.505.
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Kechida, M., R. Mesfar, R. Klii, S. Hammami, and I. Khochtali. "PS6:128 Influence of associated auto immune diseases in systemic lupus erythematosus." 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.171.
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Adil Mansoor, AL-Husnah. "Role of Interleukin-35 In The Pathogenesis of Hashimoto’s Thyroiditis Disease." In X INTERNATIONAL CONGRESS OF PURE AND APPLIED TECHNOLOGICAL SCIENCES. Rimar Academy, 2023. http://dx.doi.org/10.47832/minarcongress10-1.
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The immune system has the ability to distinguish between self and non-self. Also, Regulatory T-cells are a portion of Tcells that are in charge of preserving regulation of the immune system and immune tolerance through active immunerepression. Immune tolerance is very important to prevent the immune system from interacting against itself and thus to avoid the development of autoimmune diseasesInterleukin-35 (IL-35), which is a member of the interleukin-12 (IL12) cytokine family, is an anti-inflammatory immune response that plays the important function in the obstruction of the development of autoimmune diseases in different tests autoimmunities. When loss of self-tolerance occurs becuses many genetic and environmental factors, this causes the absence of balanced anti-inflammatory immune responses, which reduces the in vivo suppressive capacity of Treg, which is taken to be a regular T-cell-linked autoimmune disease., especially Hashimoto’s thyroiditis (HT). Methods: The current study included 90 samples. 60 hypothyroid HT patients (Group 1) and 30 healthy controls (Group 2) were enrolled in the study. Blood samples were collected and separated into serum from the two groups to be used to measure the functions of the thyroid gland by measuring the levels of thyroid hormone and thyroid stimulating hormone, measuring the level of anti-thyroid auto-antibodies, and determining the standard of serum Interloukin-35 through ELISA. Results: The results of the current study Through statistical analysis using the program SPSS version 22, it was shown that serum IL-35 levels were inversely Correlation used Pearson test with TSH, TPO-Ab, and TG-Ab in patients HT (-.292 (P≥0.01), -.245 (P≥0.02), -.269 (P≥0.01). While serum IL-35 levels were directly correlated with TSH, TPO-Ab, and TGAb in healthy controls (.151 (P≥0.01),.192 (P≥0.01),.097 (P≥0.01). The results of the current study showed a highly significant difference in TSH and FT4, respectively (P≥0.01), between the control and hypothyroid groups. Hypothyroidism is more common in females than males, and the incidence of hypothyroidism steadily increases with advancing age. Thyroid hormone concentrations show a significant change in patients with hormonal hypothyroidism compared with the control group. Conclusion: Our findings indicate an effective role for interleukin 35 in the reverse association with auto-antibodies and the development of autoimmune diseases, especially Hashmoto's disease
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Scherlinger, M., J. Lutz, J. Sibilia, E. Chatelus, and M. E. Truchetet. "SAT0499 Association between systemic sclerosis and other systemic auto-immune diseases: study in two university hospitals cohorts." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2227.
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Scherlinger, Marc, Philippe Mertz, Flora Sagez, Alain Meyer, Renaud Felten, Emmanuel Chatelus, Rose-Marie Javier, et al. "O5 Worldwide trends in all-cause mortality of auto-immune systemic diseases between 2001 and 2014." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.19.
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Bussel, J. "FOR MODULATION AS A MEANS OF ELEVATING THE PLATELET COUNT IN ITP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644761.
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ITP is an autoantibody-mediated disease which would logically be treated by decreasing the level of autoantibody. However, the most exciting developments in understanding the pathophysiology of the thrombocytopenia and its treatment involve a better understanding of the MPS FcR system and ways in which it can be modulated. This work has focussed on phagocytic paralysis or FcR blockade (FcRBl): the slowing of destruction of antibody-coated platelets despite the persistent presence of antibody on the surface of the platelet.Several areas have been explored in learning about the MPS system. Investigation by Kurlander among others have revealed that at least 2 FcR's exist on mononuclear phagocytes: one with high and one with low affinity for monomeric IgG. Study of the high affinity FcR expressed by circulating monocytes, by Schreiber among others, has explored the effect of Danazol to decrease the expression of this FcR. The clinical relevance of this receptor is uncertain however because it is saturated in vitro by physiologic concentrations of IgG. Unkeless defined the properties of the low affinity "immune complex" FcR, expressed on macrophages and neutrophils, via monoclonal antibody 3G8 (see below) which blocks ligand binding to this FcR. The exact roles of these two, and possibly more, FcR's are being explored. Another still unsolved controversy involves whether the interaction Fc portions of antibodies coating particles with FcR's is mediated by a conformational change of the Fc portion or by a multipoint attachment of several Fc parts.Studies by Mollison in the 60's demonstrated that the MPS had a limited capacity for removal of antibody-coated (red) cells. Shulman pursued MPS modulation by exploring the inhibition of thrombocytopenia caused by infusion of ITP plasma into normals. Kelton demonstrated that "compensated" ITP may be caused by a decreased clearance of antibody-coated cells and that the rate of clearance of antibody-coated cells may be correlated with rate of clearance of antibody-coated cells may be correlated with the intrinsic levels of IgG. Stossel investigated FcRBl as a mechanism of effect of corticosteroids and related it clinically. Subsequently intravenous gammaglobulin (IVGG) was introducedas a treatment of ITP and Fehr et al first demonstrated FcRBl as the mechanism of effect of IVGG. Exploration of the mechanism of the FcRBl caused by IVGGled Salama and Mueller-Eckhardt to demonstrate the therapeutic effect of I anti-D, which apparentlycoats RBC with antibody and causes their destruction atthe coats RBC with antibody and causes their destruction at the expense of antibody-coated platelets. A similar degree of FcRBl has been shown for aldometrelated to the development of antibody on RBC.Our studies, including Drs. Clarkson, Kimberly, Nachman, and Unkeless, have focussed on the role of the low affinity or "Immune complex" FcR by using monoclonal antibody 3G8 in vivo. An infusion of 1 mg/kg of 3G8 in chimpanzees caused a reproducible FcRBl demonstrable by a slowing of the destruction of antibody-coated RBC for > 10 days (JEM, 1986). Less effect of 3G8 to inhibit CIC removal was seen using DNA-anti-DNA as the immune complex. In view of the wel1-documented effects of IVGG infusion to create FcRBl, we infused 3G8 into 6 adults with refractory ITP (NEJM, 1986). Specifically these patients were refractory to all forms of conventional therapy including splenectomy, steroids, vinca alkaloid infusion, immunosuppressives and danazol . 3 of the 6 patients had peak platelet responses to >80,000/ul. The other 3 had short-lived platelet increases from 10 to 30,000/ul. These responses confirmed the effect of FcRBl, specifically of the low affinity FcR, to underlie a dramatic platelet increase in therapy of ITP. Surprisingly 3 of the patients had apparent longterm effects of this therapy demonstrable in 2 cases as a maintenance of the platelet count >20,0C0/ul without any further therapy and in 1 case as a clearly enhanced responsiveness to other therapies following 3G8 infusion. Since Natural Killer activity was (transiently) ablated by 3G8 infusion, we speculate that an alternation of regulation of (auto) antibody production by NK cells may be responsible for this effect and that FcR interactions include regulatory roles in addition to their primary function of removal of CIC.
Reports on the topic "Systemic Auto-Immune Disease"
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LI, jianhong, Zhuang LI, Yalin SHE, and Guohua LIN. Assessment of acupuncture for treating herpes zoster:a protocol for an umbrella systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0010.
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Review question / Objective: Patients who suffer from HZ in line with the consensus of Chinese experts will be included, regardless of sex, race and time of onset . Those who diagnosed with PHN, auto-immune diseases, pregnant women will be excluded.Acupuncture, electroacupuncture, fire needle, skin acupuncture, plum blossom needle, auriculo-acupuncture all these such therapies in treating herpes zoster will be included.The control group’s treatment includes drug therapy (such as antiviral acyclovir nutritional nerve medicine or traditional Chinese medicine, etc.) ，sham acupuncture, placebo, no treatment, and so on except acupuncture therapy. efficacy rate (with reference to the guiding principles of Clinical Research of New drugs in China (trial)).pain evaluation (pain relief time, pain intensity, visual analogue score, VAS), incidence of residual neuralgia PHN.
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Wongpiyabovorn, Jongkonnee, Nattiya Hirankarn, Yingyos Avihingsanon, Tewin Tencomnao, Yong Poovorawan, and Kriangsak Ruchusatsawat. The association between immunogenetics and genetic susceptibility of psoriasis in Thai population. Chulalongkorn University, 2006. https://doi.org/10.58837/chula.res.2006.27.
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Psoriasis is T-cell-mediated skin autoimmunity, required environmental triggers and genetic susceptibility factors to become manifested. Psoriasis is a chronic skin disease characterized by the abnormal hyperproliferation and differentiation of the epidermis, elongated and prominent blood vessels and a thick perivascular lymphocytic infiltrate. Vascular endothelial growth factor (VEGF) gene play important role in pathogenesis of various diseases with angiogenic basis such as breast cancer and autoimmune disease including psoriasis. Many studies analyzed the association of VEGF gene polymorphism in many positions in Caucasian and non-Caucasian. Most reports in some position that really point to important about single nucleotide polymorphism (SNP) with several autoimmune diseases including psoriasis. Although the precise causes of this auto-immune disease remain elusive. It appears to be influenced by stress. The serotonergic system known to depend primarily on the serotonin transporter (5-HTT) may have a role in psoriasis. The serotonin transporter-linked promoter region (5-HTTLPR) polymorphism occurred by insertion/deletion is evident to result in three different length alleles namely S, L as predominant variant alleles and XL as a rare one. These three alleles have 14, 16 and 18 or 20 repetitive DNA sequences, respectively and have been shown to associate with certain neuropsychiatric diseases. Although roles of serotonin and serotonin receptors in psoriasis were investigated, the impact of 5-HTTLPR on psoriasis has not been studied. Therefore, the 5-HTTLPR polymorphism was analyzed to assess whether these variants are associated with psoriasis. Furthermore, having recognized the relationship between oxidative stress and psoriasis, the association between G82S polymorphism in the gene encoding the receptor for advanced glycation end products (RAGE) and psoriasis was investigated. The aims of study, we determine the distribution of VEGF, RAGE and 5-HTTLPR polymorphism in Thai psoriasis patients. We analyzed SNPs within the VEGF (-1557) (C/A), -460(C/T) and +405(C/G)). G82S RAGE and 5-HTTLPR (S, L and XL) gene polymorphism. In population-based case-control study, allele and genotype frequencies of each marker were compared between 234 unrelated healthy volunteers and 154 chronic plapue psoriasis patients (102 early-onset and 52 late-onset psoriasis) for VEGF gene, one hundred seventy eight healthy donors and 134 psoriasis patients for RAGE gene and one hundred twenty seven healthy controls and 142 psoriasis patients for 5-HTTLPR gene. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-sequence specific primer (PCR-SSP) methods. The results, The -460 TT or CT compared to CC VEGF genotype were found to be significantly risk associated with early-onset psoriasis patients compared with healthy controls (p=0.0450, odds ratio (OR) =4.67, 95% confidence interval (CI) = 1.03-29.52). Interesthingly, haplotype analysis revealed that the CTG haplotype was found to be significantly associated with susceptibility to psoriasis and early-onset psoriasis compared with healthy controls (p=0.0460, OR=1.37, 95% CI=1.00-1.87, p=0.0163, OR=1.54, 95% CI=1.08-2.18, respectively). Moreover, VEGF plasma concentration was not significantly different between groups of haplotype in psoriasis patients. A significantly greater 82A G82S RAGE allele frequency was observed in psoriatic patients than in control subjects (p=0.001 OR=0.52 95% CI=0.35-0.78). Finally, the 5HTTPR polymorphism was no significant change in the allelic frequencies between psoriatic and control subjects (p=0.531, OR=1.15, 95% CI=0.78-1.70). Thus, the result demonstrated that the CTG haplotype and -460 C/T VEGF polymorphism may be used as a genetic marker for early-onset psoriasis in Thais but the 5-HTTLPR was not associated with psoriasis in Thai population. Furthermore, the G82S RAGE polymorphism was associated with psoriasis, and further investigations should be carried out to gain insights into its molecular mechanism in psoriasis.