The Experts below are selected from a list of 256818 Experts worldwide ranked by ideXlab platform
Harvey Cantor - One of the best experts on this subject based on the ideXlab platform.
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Regulatory T cells subdue an Autoimmune Disease
Nature, 2019Co-Authors: Harvey CantorAbstract:A type of immune cell called a CD8 T cell, which usually kills Disease-causing agents, has been found instead to suppress self-reactive immune cells, thereby offering protection against an Autoimmune Disease in mice. CD8 T cells can suppress self-reactive CD4 T cells in mice.
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molecular mimicry by herpes simplex virus type 1 Autoimmune Disease after viral infection
Science, 1998Co-Authors: Zi Shan Zhao, Francesca Granucci, Priscilla A Schaffer, Harvey CantorAbstract:Viral infection is sometimes associated with the initiation or exacerbation of Autoimmune Disease, although the underlying mechanisms remain unclear. One proposed mechanism is that viral determinants that mimic host antigens trigger self-reactive T cell clones to destroy host tissue. An epitope expressed by a coat protein of herpes simplex virus–type 1 (HSV-1) KOS strain has now been shown to be recognized by autoreactive T cells that target corneal antigens in a murine model of Autoimmune herpes stromal keratitis. Mutant HSV-1 viruses that lacked this epitope did not induce Autoimmune Disease. Thus, expression of molecular mimics can influence the development of Autoimmune Disease after viral infection.
Ann Marshakrothstein - One of the best experts on this subject based on the ideXlab platform.
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toll like receptors in systemic Autoimmune Disease
Nature Reviews Immunology, 2006Co-Authors: Ann MarshakrothsteinAbstract:Toll-like receptors (TLRs) have a crucial role in the early detection of pathogen-associated molecular patterns and the subsequent activation of the adaptive immune response. Whether TLRs also have an important role in the recognition of endogenous ligands has been more controversial. Numerous in vitro studies have documented activation of both autoreactive B cells and plasmacytoid dendritic cells by mammalian TLR ligands. The issue of whether these in vitro observations translate to an in vivo role for TLRs in either the initiation or the progression of systemic Autoimmune Disease is a subject of intense research; data are beginning to emerge showing that this is the case.
Paul Hasler - One of the best experts on this subject based on the ideXlab platform.
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Biological therapies directed against cells in Autoimmune Disease
Springer Seminars in Immunopathology, 2006Co-Authors: Paul HaslerAbstract:Among the cells of the immune system involved in the pathogenesis of Autoimmune Disease, T cells have received the most attention. The central role of these cells in several animal models of Autoimmune Diseases and in human Disease counterparts has provided the rationale for specific therapeutic targeting of T cell subsets, especially CD4 T cells. So far, the applicability of this approach has not been clearly evident in clinical trials, which was also the case when nondepleting “coating” anti-CD4 monoclonal antibodies was used. In the past several years, experimental evidence supporting a major role of B cells in systemic Autoimmune Disease has grown. This includes the pathogenicity of certain autoantibodies, the potential of B cells to present antigen in the context of MHC Class II and to signal via costimulatory molecules, and to secrete proinflammatory cytokines. In some instances, engagement of the B cell receptor and other surface receptors is sufficient to stimulate B cells to produce antibodies. The depletion of B cells by targeting the surface marker CD20 has been shown to be effective in treating rheumatoid arthritis with a good side effect profile. Series of cases with other systemic Autoimmune Diseases indicate that this strategy may be effective in these conditions too. The clinical data add weight to the importance of B cells in the pathogenesis of Autoimmune Diseases.
Dragomir Marisavljevich - One of the best experts on this subject based on the ideXlab platform.
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Stress as a trigger of Autoimmune Disease.
Autoimmunity reviews, 2007Co-Authors: Ljudmila Stojanovich, Dragomir MarisavljevichAbstract:The etiology of Autoimmune Diseases is multifactorial: genetic, environmental, hormonal, and immunological factors are all considered important in their development. Nevertheless, the onset of at least 50% of Autoimmune disorders has been attributed to "unknown trigger factors". Physical and psychological stress has been implicated in the development of Autoimmune Disease, since numerous animal and human studies demonstrated the effect of sundry stressors on immune function. Moreover, many retrospective studies found that a high proportion (up to 80%) of patients reported uncommon emotional stress before Disease onset. Unfortunately, not only does stress cause Disease, but the Disease itself also causes significant stress in the patients, creating a vicious cycle. Recent reviews discuss the possible role of psychological stress, and of the major stress-related hormones, in the pathogenesis of Autoimmune Disease. It is presumed that the stress-triggered neuroendocrine hormones lead to immune dysregulation, which ultimately results in Autoimmune Disease, by altering or amplifying cytokine production. The treatment of Autoimmune Disease should thus include stress management and behavioral intervention to prevent stress-related immune imbalance. Different stress reactions should be discussed with Autoimmune patients, and obligatory questionnaires about trigger factors should include psychological stress in addition to infection, trauma, and other common triggers.
Kazuhiko Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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Ethnic differences in allele frequency of Autoimmune-Disease-associated SNPs
Journal of Human Genetics, 2005Co-Authors: Mikako Mori, Ryo Yamada, Kyoko Kobayashi, Reimi Kawaida, Kazuhiko YamamotoAbstract:Several multiple, large-scale, genetic studies on Autoimmune-Disease-associated SNPs have been reported recently: peptidylarginine deiminase type 4 (PADI4) in rheumatoid arthritis (RA); solute carrier family 22 members 4 and 5 (SLC22A4 and 5) in RA and Crohn’s Disease (CD); programmed cell death 1 (PDCD1) in systemic lupus erythematosus (SLE), type 1 diabetes mellitus (T1D), and RA; and protein tyrosine phosphatase nonreceptor type 22 (PTPN22) in T1D, RA, and SLE. Because these reports on association were not always evaluated in multiple ethnic groups and because ethnic difference in allele frequency of the variants has been also reported, we investigated allele frequencies of nine SNPs in four Autoimmune-Disease-associated loci in Caucasian, African-descent, and Japanese populations. Although SNPs in PADI4 had similar allele frequency among three groups [maximal difference 11%; (P >0.05)], the other three loci revealed statistically significant allele frequency differences (maximal difference 39% (P
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ethnic differences in allele frequency of Autoimmune Disease associated snps
Journal of Human Genetics, 2005Co-Authors: Mikako Mori, Ryo Yamada, Kyoko Kobayashi, Reimi Kawaida, Kazuhiko YamamotoAbstract:Several multiple, large-scale, genetic studies on Autoimmune-Disease-associated SNPs have been reported recently: peptidylarginine deiminase type 4 (PADI4) in rheumatoid arthritis (RA); solute carrier family 22 members 4 and 5 (SLC22A4 and 5) in RA and Crohn’s Disease (CD); programmed cell death 1 (PDCD1) in systemic lupus erythematosus (SLE), type 1 diabetes mellitus (T1D), and RA; and protein tyrosine phosphatase nonreceptor type 22 (PTPN22) in T1D, RA, and SLE. Because these reports on association were not always evaluated in multiple ethnic groups and because ethnic difference in allele frequency of the variants has been also reported, we investigated allele frequencies of nine SNPs in four Autoimmune-Disease-associated loci in Caucasian, African-descent, and Japanese populations. Although SNPs in PADI4 had similar allele frequency among three groups [maximal difference 11%; (P >0.05)], the other three loci revealed statistically significant allele frequency differences (maximal difference 39% (P <0.00001), 13% (P <0.00001), and 8% (P <0.00001) in SLC22A4, PDCD1, and PTPN22, respectively). Of note, three SNPs in the three loci that had allele frequency more than 8% in the Caucasian population were either not polymorphic at all or extremely rare in the Japanese population. Our data suggest that ethnic variations of polymorphisms should be evaluated in detail, and differences should be incorporated into investigations of susceptibility variants for common Diseases.
