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)

The radiological changes of the cervical spine were evaluated in 57 patients with psoriatic arthritis and were correlated with clinical, radiological, and immunogenetic features of the disease. Forty patients (70%) showed radiological evidence of the cervical spine being affected by the disease. Two patterns of cervical spine abnormalities were noted. Fifteen patients (26%) had erosive and/or subluxing cervical rheumatoid like lesions; 25 patients (44%) had a more frequently reported pattern similar to ankylosing spondylitis. Although subaxial subluxations were the most frequently observed cervical abnormalities (53%) in the inflammatory subgroup, none of the patients studied had cord compression. Ankylosing cervical spine disease was the only form of axial involvement in nine (36%) of 25 patients with the ankylosing form of psoriatic arthritis. All of these patients had peripheral disease and were B27 negative. Predictors of cervical spine disease patterns were considered using clinical, demographic, and radiological features and HLA antigens. The results of a multivariate analysis showed that the best predictors of inflammatory cervical spine disease are the presence of HLA-B39 and HLA-DR4 antigens, radiocarpal erosions, and the absence of the HLA-DR5 antigen.
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PMID:The cervical spine in patients with psoriatic arthritis: a clinical, radiological and immunogenetic study. 154 41

There is convincing evidence of a genetic basis for both psoriasis and psoriatic arthritis (PsA). Part of this genetic predisposition is due to genes within the major histocompatibility complex (MHC). In psoriasis, the primary association is with HLA-Cw6. Further work on specific nucleotide frequencies, especially those in the alpha 1 domain helix of the HLA-C molecule, will be of interest in determining whether a specific nucleotide frequency is present in all patients. The situation in PsA is considerably more complex. It is now established that there is an association between HLA-B27 and PsA, both in its peripheral arthropathy and in spinal disease in which radiological sacroiliitis is present. Spinal disease without radiological sacroiliitis is probably not associated with HLA-B27. There is some suggestion that HLA-B16 or its splits, HLA-B38 and HLA-B39, may also be associated with PsA, but there is considerable heterogeneity between the series, which prevents a firm conclusion being made. It is possible, but again not conclusive, that there is an association between HLA-DR4 and the symmetrical seronegative pattern of peripheral PsA. It is also likely that genes outwith the MHC predispose to psoriasis and PsA. It is further likely that a role will be found for environmental factors in both psoriasis and PsA. There is a tantalizing possibility of a complex interplay between a variety of environmental factors and genetic factors, both within and outwith the MHC, determining not only susceptibility but also the individual clinical pattern of disease. Further clarification of these possibilities is likely to depend primarily on understanding the role of genes within the MHC in predisposing to comparatively more homogeneous diseases, such as psoriasis and ankylosing spondylitis, before the mechanisms operating in PsA can be analysed and better understood.
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PMID:Psoriatic arthritis. Genetics and HLA antigens. 807 87

The arthritogenic peptide hypothesis has inspired research aimed at defining the peptide-presenting properties of HLA-B27 subtypes and their relation to ankylosing spondylitis. Various studies have shed new light on the influence of HLA-B27 polymorphism in modulating peptide binding and T-cell antigen presentation. Moreover, multiple factors along the antigen processing-loading pathway, including tapasin, contribute to shaping the HLA-B27 repertoire. Other studies have revealed significant peptide-binding similarities between HLA-B27 and subtypes of HLA-B39, supporting a role of this antigen in spondyloarthropathy. A putative pathogenetic role of the HLA-B27 heavy chain, initially suggested from studies in transgenic mice, is claimed on the basis of novel, yet circumstantial, evidence concerning an apparently unusual capacity of the heavy chain to form stable homodimers or misfold after biosynthesis. Finally, it appears that arthritogenic infections might downregulate HLA-B27 expression, favoring bacterial survival. The specificity and mechanism of this phenomenon are yet to be defined.
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PMID:HLA-B27 and immunogenetics of spondyloarthropathies. 1091 Jan 75