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)

HLA-D typing of 44 patients with ankylosing spondylitis (AS) and 31 patients with Reiter's syndrome (RS) did not show increased frequency of any particular Dw allele in either population of patients as compared to controls. Such studies also allowed each patient's general response to be compared with other general responses within each experiment. Contrary to reports of diminished lymphocyte responses in AS patients, hyperresponsiveness in both AS and RS patients was found.
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PMID:HLA-D locus typing in ankylosing spondylitis and Reiter's syndrome. 21 95

Within the last 7 years, HLA and disease studies have made it clear that most of the diseases previously known to be HLA-A- or B-associated do in fact show stronger associations with HLA-D/DR antigens. This observation strengthens the assumption that Ir and/or Is determinants are responsible for these associations in agreement with the fact that many of these diseases are characterized by autoimmune phenomena. However, some diseases, ankylosing spondylitis in particular, still show stronger associations with HLA-ABC than with DR antigens. Among the conditions which have been shown to be HLA-associated more recently, four deserves special mention: (i) maternal immunization against the Zwa antigen because this is a good candidate for an antigen-specific Ir gene action; (ii) IgA deficiency in blood donors because this is a non-antigen-specific immunodeficiency; (iii) idiopathic hemochromatosis and (iv) congenital adrenal hyperplasia due to 21-OH deficiency because immune mechanisms are unlikely to be involved. HLA studies and new genetic methodology have significantly advanced our knowledge about the inheritance of some diseases. Thus, HLA-B27 or a B27-associated HLA factor confers a dominant susceptibility to ankylosing spondylitis. HLA plays a definite and strong role in the susceptibility to IDDM, but simple genetic models (dominant, recessive, and intermediate) have been made unlikely on the basis of HLA results; the hypothesis that there are two different susceptibility genes within the HLA system still remains viable, but the demonstration of clinical heterogeneity and/or (better) of different pathogenetic pathways for DR3- and DR4-associated IDDM is required to substantiate it.
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PMID:HLA and disease 1982--a survey. 633 68

Despite many reports on the association between ankylosing spondylitis and HLA-B27, most studies have failed to find a significant relationship between HLA-A or B antigen and rheumatoid arthritis. Stastny, however, showed a significantly high frequency of HLA-Dw4 in rheumatoid arthritis in 1976. The study of HLA antigens in Japanese patients with rheumatoid arthritis are thought to be significant in view of the pathogenesis of disease. Eighty-eight Japanese patients with "definite" or " classical" rheumatoid arthritis according to the ARA criteria and 104 normal individuals were typed for serologically detectable HLA-A, B, C, and D antigens. Though small discrepancies were observed in several of the HLA-A, B, and C, antigens, they were not definitely significant. The frequency of HLA-DR4 increased to 70.5% in patients compared to 46.1% in the control (i.e. normal) group (p less than 0.001). However, the frequency increased to 80.6% in male patients (p less than 0.0005). Of interest was the significantly high frequency of HLA-DR4 in males, compared to the low frequency of HLA-DR2 (p less than 0.02). Rheumatoid patients were subdivided into different groups according to the year of onset, the presence of the the rheumatoid factor or rheumatoid nodules, the functional grade and treatment. There were no significant differences in the frequency of HLA-DR4 among subgroups. The results indicate that rheumatoid arthritis, especially in males, is associated with genes of the HLA-D region and that immunogenetic factors linked to HLA have an important role in its pathogenesis.
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PMID:[[HLA in rheumatoid arthritis (author's transl)]. 728 33