Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When studying heterogeneity of B27-positive disease versus B27-negative disease, very different patterns of disease associations but also a lot of similarities may be observed. In general, B27-positive disease has an earlier onset, a more severe and prolonged clinical course and is more often complicated by acute anterior uveitis and peripheral arthritis, whereas B27-negative disease is accompanied by psoriasis, inflammatory bowel disease and erythema nodosum in a higher percentage of the cases. Despite these differences, B27-positive disease may be completely undistinguishable from B27-negative disease in a number of individual cases. Family aggregation and male preponderance, however, are only seen in B27-positive disease. These observations may lead to the conclusion that HLA-B27 is probably not the only key to the pathogenesis of these diseases, but nevertheless an important genetic factor in disease expression.
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PMID:B27+ disease versus B27- disease. 225 79

Every HLA antigen, as defined by the WHO-HLA Nomenclature, is unique. The major function of these molecules is to present antigen-peptides to the T-cell receptor, thereby contributing to the immunological defence mechanism. This function is regulated for each MHC antigen by its unique structure, with the peptide-binding pockets of the three-dimensional groove of the corresponding molecules playing the critical role. However, HLA-B27 is special by virtue of its disease association(s). Various aspects which might provide an explanation for--or at least a clue to an understanding of the specific role of--B27 in its disease associations are reviewed. Since it appears that there are no published experimental data which would support either of the alternative hypothetical possibilities, the bulk of current theories must therefore be purely speculative. The only lead to a better understanding of the function of B27 in disease associations is the postinfectious reactive arthritis. If it is the B27 molecule itself which is involved, further in vivo work on B27 transgenic animals might help solve this problem with its numerous unknown factors.
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PMID:Dysfunction of HLA-B27. 225 89

HLA-B*2705 transgenic mice were continuously backcrossed to mice of the B10 background with various haplotypes. A high level of expression of the HLA-B27 protein was detected on peripheral blood lymphocytes (PBLs) from mice homozygous for H-2b, H-2f, H-2s, H-2p, H-2r, and H-2k haplotypes by FACS analysis with the ME-1 antibody. A lower level of expression of B27 was observed on PBLs from H-2v mice. Little or no expression of B27 was detected on PBLs from H-2 or H-2d mice. We hypothesize that the HLA-B27 heavy chain is analogous to and competes with endogenous class I heavy chains in the H-2d, H-2q and H-2v haplotypes. Interestingly, other studies in our laboratory have demonstrated that mice with the H-2d and H-2q haplotypes with deletions of certain T cell receptor subsets are more prone to Yersinia-induced arthritis (YIA). Therefore, the mouse model of YIA may provide insights into the mechanisms of HLA-B27-linked spondyloarthropathies in man.
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PMID:Effect of H-2 genes on expression of HLA-B27 and Yersinia-induced arthritis. 225 92

Patients with juvenile spondyloarthropathy who carry HLA B27 antigen or have a family history of ankylosing spondylitis may have marked tarsometatarsal arthritis. This may be associated with hindfoot involvement and result in a supination deformity. Spontaneous fusion with complete obliteration of the tarsometatarsal joints may occur.
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PMID:Tarsometatarsal involvement in juvenile spondyloarthropathy. 226 14

It should again be cautioned that these hypotheses are just that--hypotheses, for which there are some suggestive but not conclusive data. I have described these hypotheses using B27 and AS, and DR4 and RA. We are all aware that AS occurs in individuals who are B27 negative, and RA occurs in individuals who lack DR4. Although space does not permit further elaboration here, these hypotheses can be modified to take these additional associations into account. It should also be noted that even if the mechanisms advanced in these hypotheses prove to be true, different mechanisms may apply to different diseases, and several of these mechanisms may act in concert to produce disease. Nevertheless, these hypotheses provide a framework against which future experiments can be designed to further elucidate the relationship among infectious agents, immunity, and rheumatic diseases.
Arthritis Rheum 1990 Apr
PMID:Infectious agents, immunity, and rheumatic diseases. 232 27

The present study describes the profile of seronegative spondarthritides (SSA) in young servicemen. SSA was diagnosed in 63 patients from a prospective study on spondyloarthropathy. The SSA group consisted of ankylosing spondylitis (AS, 40 patients), Reiter's syndrome (RS, 6) and SSA undifferentiated (SSA-U, 17). The chief clinical and radiological features of the group were due to sacro-iliitis/spondylitis, peripheral arthritis and enthesopathy. Except for RS, extra-articular features were sparse. Mucosal lesions were not evident. Radiologically, sacro-iliitis varied from 24% in SSA-U to 100% in AS, and was disproportionately less when compared to its clinical extent. Dominant lower limb arthritis (poly and oligo) was seen in AS (40%), SSA-U (88.2%) and RS (100%). HLA A and B were typed in patients and controls. HLA AI had a significant negative association (p less than 0.05) with AS and the SSA group, and its relative risk (R) was consistently low (0.2-0.3). HLA B27 was present in 65.7%, 73%, 67%, 41% and 9% of the SSA group, AS, RS, SSA-U and controls respectively (p less than 0.05). Significant R values of A and B loci antigens in disease groups are presented. When compared with available Indian literature, this study highlights the variability and overlap in the disease. Disease markers currently available have limitations in defining the various subsets of SSA.
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PMID:Spectrum of seronegative spondarthritides (SSA) with special reference to HLA profiles. 238 18

One hundred and eighty-one patients attending a dermatology clinic were studied. Twenty-two (12%) were B27 positive. Twenty had peripheral psoriatic arthritis; 3 of these showed sacroiliitis (1 B27 positive, 2 B27 negative). Only one of the other 161 patients had sacroiliitis and he was B27 positive. Subsequently we examined 54 consecutive patients with psoriatic arthritis: 51 had peripheral arthritis (6 with sacroiliitis) and 3 exclusively axial involvement (2 sacroiliitis, one syndesmophytes with normal sacroiliac joints). All patients were pooled together and divided in 4 groups: B27 positive and negative, with or without peripheral arthritis. HLA-B27 and/or peripheral arthritis were associated with an increase in axial involvement. Patients lacking both B27 and peripheral arthritis did not have sacroiliitis and only in one case showed evidence of spinal disease (0.7%). Half of the patients with peripheral arthritis and spinal involvement were B27 positive. All 3 B27 positive patients without peripheral arthritis and with spinal disease were men and they all had bilateral sacroiliitis, indistinguishable from idiopathic ankylosing spondylitis (AS). HLA-B27 and peripheral arthritis appeared to act as separate factors that increased the risk of spinal arthritis in patients with psoriasis. The effect of B27 on psoriasis appeared to be detected in 2 different ways: as a coincidental factor increasing the risk of idiopathic AS (as for the general population) or as one of the multiple HLA associations that increase the risk of psoriatic arthritis; in this latter case the spinal involvement could occur as another manifestation of the clinical course of the disease.
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PMID:Sacroiliitis in psoriasis: relationship to peripheral arthritis and HLA-B27. 238 2

The majority of patients with reactive arthritis have the major histocompatibility complex class I gene HLA-B27. The development of arthritis in these patients often occurs following infection with one of several enteric bacteria, including Yersinia enterocolitica. In this study, transgenic mice expressing HLA-B27 and their negative full sibs were infected intravenously with Yersinia enterocolitica 0:8 WA in an attempt to develop an experimental model of reactive arthritis. To date, no reactive arthritis has been observed; however, a significantly higher incidence of paralysis was observed in the HLA-B27+ transgenic mice. Injection of 10(5) organisms induced hind limb paralysis in 8 out of 30 of the HLA-B27 transgenic mice (27%) and in only 1 of the 24 negative siblings (4%). Paralysis occurred in 14 out of 30 HLA-B27+ mice (47%) at a dose of 10(4) organisms. Only 2 of the 25 negative siblings (8%) were affected at this dose. Paraspinal abscesses were found in all of the paralyzed animals. At the 10(4) dose most of the HLA-B27+ mice (70%) succumbed to the disease within 4 weeks, while the mortality in their B27- full sibs was less than 10%. Thus, HLA-B27 transgenic mice have higher mortality and morbidity from infection with Y. enterocolitica 0:8 WA than corresponding HLA-B27- littermates.
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PMID:Susceptibility of HLA-B27 transgenic mice to Yersinia enterocolitica infection. 239 Dec 53

Several forms of seronegative polyarthritis are strongly associated with HLA-B27, and a number of microorganisms have been implicated in the etiology of these diseases. To explain the association between HLA-B27 and arthritis initiated by infection with these organisms, it has been proposed that there is immunologic cross-reactivity between the B27 molecule and 1 or more microbial antigens, and that this cross-reactivity leads to tolerance to such infection and/or to the production of anti-HLA-B27 cross-reactive antibodies. Such cross-reactive antibodies were detected in the sera of only 2 of 63 patients recently infected with Shigella flexneri, Campylobacter jejuni, or Yersinia enterocolitica who had highly significant antibody levels against the infecting bacterial species. Most striking was the absence of anti-HLA-B27 antibody in the serum of 16 of 17 patients who developed reactive arthritis following Yersinia infection.
Arthritis Rheum 1986 Mar
PMID:Anti-HLA-B27 antibodies in sera from patients with gram-negative bacterial infections. 242 39

We compared in vitro lymphocytotoxicity (LCT) of peripheral blood lymphocytes (PBL), obtained from patients with ankylosing spondylitis (AS) and normal controls (NC). Assays were performed with antibacterial antisera prepared from AS- and NC-derived Klebsiella and coliforms Escherichia coli. LCT assessed by eosin staining was not significantly different in PBL of 12 AS patients and 28 controls when reacted with 3 Klebsiella and 1 E coli antisera. LCT assessed by 51Cr release was not significantly different for PBL of 20 age- and sex-matched pairs of AS patients and NC when reacted with 3 Klebsiella and 1 E coli antisera. Similarly, LCT-51Cr of PBL of 15 matched AS and NC pairs was not significantly different for anti-K21, a serotype putatively implicated in Klebsiella-HLA-B27 antigenic cross-reactivity. Our results do not support the notion of molecular mimicry between Klebsiella and B27 in the pathogenesis of primary AS.
Arthritis Rheum 1986 Mar
PMID:Normal anti-Klebsiella lymphocytotoxicity in ankylosing spondylitis. 242 40


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