Pathogenetic mechanisms in B27 associated diseases.
Various aspects of pathogenesis, or more broadly, aetiopathogenesis, in the field of B27 related disorders are considered. The main conclusions can be expressed as follows: Genetic factors are involved in the causation of the spondarthritides, although there is still controversy within individual disorders concerning the precise mode of inheritance. For instance, in some conditions evidence appears stronger for a Mendelian mechanism, in others for a multifactorial process. The mode of the HLA-B27-receptor interaction is not yet fully established, but there is strong support for the one gene cross-tolerance theory, in ankylosing spondylitis at least. It is likely that environmental factors 'collaborate' with genetic factors in causing spondarthritic disease. The factors in the environment have yet to be proved, but there is some evidence that micro-organisms such as Klebsiella and Yersinia are involved (e.g. ankylosing spondylitis, Reiter's disease, reactive arthritis). Of noninfective environmental factors, trauma could play a part, as suggested by the mode of onset and pattern of development of some examples of ankylosing spondylitis and psoriatic arthritis.
D000818:Animals; D001168:Arthritis / Q000209:etiology; D016918:Arthritis, Reactive / Q000209:etiology; D001528:Behcet Syndrome / Q000209:etiology; D005260:Female; D006680:HLA Antigens / Q000235:genetics; D015796:HLA-B27 Antigen; D000882:Haplorhini; D006801:Humans; D008023:Ligaments, Articular / Q000473:pathology; D008297:Male; D008954:Models, Biological; D011565:Psoriasis / Q000150:complications; D013167:Spondylitis, Ankylosing / Q000209:etiology* / Q000235:genetics / Q000276:immunology
D006680:HLA Antigens; D015796:HLA-B27 Antigen