Immunopathogenesis of ankylosing spondylitis

Kenna, Tony J. & Brown, Matthew A. (2013) Immunopathogenesis of ankylosing spondylitis. International Journal of Clinical Rheumatology, 8(2), pp. 265-274.

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Ankylosing spondylitis is a model immunogenetic disease with major common and rare genetic risk factors, likely environmental contributors to its pathogenesis and, to date, no treatment that has been shown to induce disease remission in long-term studies. The discovery of the association of HLA-B27 with the disease in the early 1970s triggered extensive efforts to elucidate the mechanism of this association. However, the precise role of HLA-B27 in ankylosing spondylitis pathogenesis remains unclear. In recent years, rapid progress made in the discovery of non-MHC genes involved in susceptibility to ankylosing spondylitis has combined with increasing ability to investigate the immune system to make rapid progress in unraveling the etiopathogenesis of the condition. © 2013 Future Medicine Ltd.

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ID Code: 89286
Item Type: Journal Article
Refereed: Yes
Keywords: ankylosing spondylitis, antigen processing, HLA-B27, inflammation, innate immunity, T cell, beta 2 microglobulin, dectin 1, dectin 2, HLA antigen class 1, HLA B27 antigen, interleukin 1 receptor type II, interleukin 12 receptor, interleukin 17, interleukin 22, interleukin 23, interleukin 6 receptor, killer cell immunoglobulin like receptor, tumor necrosis factor inhibitor, allele, antigen expression, antigen function, CD4+ T lymphocyte, CD8+ T lymphocyte, complex formation, cytokine production, cytokine release, disease association, disease predisposition, endoplasmic reticulum, environmental factor, ERAP1 gene, fungal gene, gamma delta T lymphocyte, gene, gene function, gene interaction, genetic association, genetic risk, haplotype, human, immune system, immunogenetics, immunopathogenesis, major histocompatibility complex, mast cell, molecular mechanics, natural killer cell, neutrophil, nonhuman, priority journal, protein expression, protein targeting, psoriatic arthritis, remission, review, rheumatoid arthritis, risk factor, signal transduction, spondyloarthropathy, unfolded protein response
DOI: 10.2217/ijr.12.84
ISSN: 1758-4272
Divisions: Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
Copyright Owner: 2013 Future Medicine Ltd
Deposited On: 20 Oct 2015 02:27
Last Modified: 20 Mar 2016 23:56

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