[Pathogenesis of ankylosing spondylitis-mechanisms of disease manifestation and chronicity].
Despite intensive research during the last three decades, it is still not clear which precise mechanisms determine the interactions between host factors (HLA-B27 and other genes, cytokines, T lymphocytes) and microbial factors leading to the manifestation and chronicity of ankylosing spondylitis (AS). Rheumatologists and histopathologists have focused their interest on decoding the immune-mediated inflammatory processes and on studying new bone formation and ankylosis. Concerning the genetic basis of AS, there is considerable effort in large genome-wide and candidate gene analyses to discover new genes that are associated with AS. Moreover, such genetic studies could identify genomic regions that determine clinical manifestations and the course of disease.
Märker-Hermann
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Klinik Innere Medizin IV, Dr. Horst-Schmidt-Kliniken GmbH, Klinikum der Landeshauptstadt Wiesbaden, Aukammallee 39, 65191 Wiesbaden, Germany. Elisabeth.maerker-hermann@hskwiesbaden.de
Frauendorf
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E
Zeidler
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H
Sieper
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J
D001327:Autoimmune Diseases / Q000209:etiology / Q000235:genetics / Q000276:immunology; D001424:Bacterial Infections / Q000150:complications / Q000276:immunology; D016207:Cytokines / Q000097:blood; D005786:Gene Expression Regulation / Q000502:physiology; D020022:Genetic Predisposition to Disease / Q000235:genetics; D015796:HLA-B27 Antigen / Q000235:genetics; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D015398:Signal Transduction / Q000235:genetics; D013167:Spondylitis, Ankylosing / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D015796:HLA-B27 Antigen; D014409:Tumor Necrosis Factor-alpha