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)

Immunohistological techniques were used to identify activated T lymphocytes within the synovial membrane of patients with rheumatoid arthritis, using the monoclonal antibody (MoAb) RFT2, which identifies a 40-k dalton molecule preferentially expressed by T blasts or activated cells. Using this reagent together with a monoclonal 'cocktail' that stains all T cells, cell counts on consecutive sections of rheumatoid synovium revealed that up to 50% T lymphocytes were RFT2+ (range 9.3-50.2%, mean 25.4). Subsequent analysis using combination immunofluorescence demonstrated that over 90% of these activated cells were of the T4+ subset. Furthermore all these cells appeared to be Leu8-, suggesting that the activated population were exclusively 'true helpers' and not suppressor inducers. Studies indicated that 50% of the RFT2+ cells were positive with anti-Tac MoAb. Comparisons with tissues from other arthropathies demonstrated that this relatively high proportion of RFT2+ cells was a feature restricted to rheumatoid arthritis, although biopsies from patients with psoriatic arthritis and ankylosing spondylitis also contained activated cells. Biopsies of Reiter's syndrome, osteo-arthritis, and pigmented villonodular synovitis contained no activated cells, nor were any seen in sections of normal synovium. The presence in rheumatoid synovial membrane of activated T cells which are only of the T4+, Leu8- subset adds weight to the suggestion that local immunoregulatory dysfunction contributes to the chronic inflammation of rheumatoid arthritis.
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PMID:Activated T lymphocytes of the synovial membrane in rheumatoid arthritis and other arthropathies. 408 40

Cryostat section of synovial tissue from patients with rheumatoid arthritis, ankylosing spondylitis, osteoarthrosis, pigmented villonodular synovitis, and from a normal knee were studied by indirect immunofluorescence with guinea-pig antibodies to the intermediate filament proteins prekeratin, vimentin, and desmin. Staining for vimentin, but absence of prekeratin and desmin, was demonstrated in synovial lining cells. Antivimentin antibody also stained synovial tissue fibroblasts and vascular endothelial lining cells. The intensity of fluorescent staining for vimentin broadly correlated with cellular proliferative activity at these 3 sites.
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PMID:Intermediate filaments in synovial lining cells in rheumatoid arthritis and other arthritides are of vimentin type. 703 25

The leucocyte migration inhibition test (LMT) has been used to search for specific antigens in rheumatoid synovial tissue. Synovial samples were collected from 20 patients with rheumatoid arthritis, from 1 patient with ankylosing spondylitis, and from 1 patient with pigmented villonodular synovitis. Inhibitory material was obtained from all 21 synovia with inflammatory disease but not from the noninflammatory synovium. The tissue extracts generally caused nonspecific migration inhibition when tested against a total of 157 pairs of rheumatoid and control leucocytes. However, occasional samples did induce migration inhibition restricted to either rheumatoid or control cells. The inhibitory factor was shown to be membrane associated and of high molecular weight (greater than 10(6) daltons). The results of this extensive study do not support the conclusions drawn from earlier reports based on smaller numbers of experiments. No evidence was obtained for the existence of specific antigenic material associated with the synovial membrane in rheumatoid arthritis.
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PMID:The nonspecific inhibitory effect of synovial tissue extracts on leucocyte migration in vitro. 743 57

Most individuals seeking consultation at sports medicine clinics are young, healthy athletes with injuries related to a specific activity. However, these athletes may have other systemic pathologies, such as rheumatic diseases, that may initially mimic sports-related injuries. As rheumatic diseases often affect the musculoskeletal system, they may masquerade as traumatic or mechanical conditions. A systematic review of the literature found numerous case reports of athletes who presented with apparent mechanical low back pain, sciatica pain, hip pain, meniscal tear, ankle sprain, rotator cuff syndrome and stress fractures and who, on further investigation, were found to have manifestations of rheumatic diseases. Common systemic, inflammatory causes of these musculoskeletal complaints include ankylosing spondylitis (AS), gout, chondrocalcinosis, psoriatic enthesopathy and early rheumatoid arthritis (RA). Low back pain is often mechanical among athletes, but cases have been described where spondyloarthritis, especially AS, has been diagnosed. Neck pain, another common mechanical symptom in athletes, can be an atypical presentation of AS or early RA. Hip or groin pain is frequently related to injuries in the hip joint and its surrounding structures. However, differential diagnosis should be made with AS, RA, gout, psudeogout, and less often with haemochromatosis and synovial chondochromatosis. In athletes presenting with peripheral arthropathy, it is mandatory to investigate autoimmune arthritis (AS, RA, juvenile idiopathic arthritis and systemic lupus erythematosus), crystal-induced arthritis, Lyme disease and pigmented villonodular synovitis. Musculoskeletal soft tissue disorders (bursitis, tendinopathies, enthesitis and carpal tunnel syndrome) are a frequent cause of pain and disability in both competitive and recreational athletes, and are related to acute injuries or overuse. However, these disorders may occasionally be a manifestation of RA, spondyloarthritis, gout and pseudogout. Effective management of athletes presenting with musculoskeletal complaints requires a structured history, physical examination, and definitive diagnosis to distinguish soft tissue problems from joint problems and an inflammatory syndrome from a non-inflammatory syndrome. Clues to a systemic inflammatory aetiology may include constitutional symptoms, morning stiffness, elevated acute-phase reactants and progressive symptoms despite modification of physical activity. The mechanism of injury or lack thereof is also a clue to any underlying disease. In these circumstances, more complete workup is reasonable, including radiographs, magnetic resonance imaging and laboratory testing for autoantibodies.
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PMID:Rheumatic diseases presenting as sports-related injuries. 1893 22