Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many human diseases are associated with HLA class I, class II and class III antigens. It appears that the class III antigen disease associations can be explained by a direct defect operating at the level of either the class III gene or its gene product. The mechanism underlying class I and class II antigen disease associations is at present unknown. In this review we have considered thirty diseases which have been ranked according to their relative risk as defined by the frequency of a given HLA antigen in patient and control populations. The chronic inflammatory disorder, ankylosing spondylitis and its association with HLA B27 has been used as a model to study the HLA linked diseases. We have suggested that the disease may be caused by the Gram-negative microorganism Klebsiella which has antigenic similarity to HLA B27. It is proposed that some antibodies made against Klebsiella bind to HLA B27, thereby acting as autoantibodies leading to the pathological sequelae of chronic inflammatory arthritis. This is the crosstolerance hypothesis or molecular mimicry model and it has been compared to the receptor model. It is further suggested that the crosstolerance hypothesis can be utilised as a general theory to explain the association of other diseases with the class I and class II antigens, and offer a possible explanation for the polymorphism of HLA.
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PMID:HLA and disease. 128 96

An induced expression of class II transplantation antigens is seen on synovial cells in human arthritides such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS) as well as in some experimental animal models for arthritis, i.e. in collagen arthritis in mice and rats and in adjuvant arthritis in rats. In this paper, additional original data are presented concerning the expression of HLA-DR, DP, and DQ antigens on macrophage-like and fibroblast-like cells within the cartilage-pannus junction in RA. The functional implications of this induced synovial class II antigen expression is discussed against the background of both in vitro experiments on human synovial cells and in vivo experiments in the animal arthritis models.
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PMID:Induced expression of class II transplantation antigens in the cartilage-pannus junction in RA: chronic synovitis as a model system for aberrant T-lymphocyte activation. 304 72