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

Twenty-two patients were followed for a mean of 10.7 years after acute Yersinia arthritis. Their clinical course, agglutinating antibodies, and laboratory parameters of inflammation were analyzed. In 73% of cases HLA-B27 was positive. The acute disease lasted from 1 month to 1 year. One male patient showed a bilateral synostosis of sacroiliac joints at the acute phase of the disease. He developed the clinical characteristics of severe ankylosing spondylitis. Another two patients with HLA-B27 had radiologically inflammatory changes of sacroiliac joints or symphysis without clinical findings. Agglutinating antibodies against dead Yersinia bacilli were negative in all patients. No laboratory signs of inflammation were present. The long-term prognosis of Yersinia arthritis is benign.
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PMID:[Yersinia arthritis. Long-term follow up]. 821 19

In the spondyloarthropathies human leukocyte antigen (HLA) B27 confers a strong genetic predisposition to the development and to the chronicity of disease after extra-articular infection with certain gram-negative bacteria. The close relationships between infection, HLA-B27, other genetic factors, and the host immune system, however, still are unexplained. HLA-B27-positive arthritis continues to be an area of intensive investigation in basic and clinical research. New animal models with HLA-B27 transgenic mice and rats, as well as recent developments in understanding the processes involved in signal transduction, cytokine production, and human T-lymphocyte activation, contribute to the development of new pathogenic models of the spondyloarthropathies. This article summarizes the current concepts of the cause and pathogenesis of the spondyloarthropathies resulting from studies of clinical materials. The host-microbial interplay in human disease, namely in bacteria-induced reactive arthritis, may eludicate principle disease mechanisms in acute disease and in the development of chronic autoimmune arthritis or ankylosing spondylitis.
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PMID:Pathogenesis of human leukocyte antigen B27-positive arthritis. Information from clinical materials. 989 15