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)

The spondarthropathy (Sp)-associated HLA-B27 antigen includes at least seven subtypes, B*2701-07, of which 01, 02, 05 and 07 occur in Caucasians. This study examined the B27 subtype distribution in British patients with Sp. The 133 HLA-B27+ subjects comprised 94 European Caucasian Sp (58 ankylosing spondylitis (AS), 22 reactive arthritis (ReA; 11 sexually acquired (SARA), 11 enteric (EReA)), eight undifferentiated Sp (USp), and six pauciarticular juvenile-onset chronic arthritis (pJCA)) patients, and 34 healthy Caucasian controls, together with four Asian Indian and one Chinese. 35S-labelled B27 was immunoprecipitated with anti-B27 MoAbs, and subtyped according to isoelectric point (pI) following isoelectric focussing. The use of B27 MoAb permitted subtype assignment without full class I HLA typing. The vast majority (95%) were B*2705 (Caucasian controls 31/34; AS 55/58; ReA 21/22; USp 8/8, and pJCA 6/6; Indian control 1/1 and AS 2/3; Chinese pJCA 1/1), and the remainder B*2702. No B*2701 or 07 subjects were identified. AS occurs in both B*2702 and 05 subjects, and we extend this observation to small numbers of ReA and of Indian AS subjects. This implicates molecular features shared between B27 subtypes, rather than subtype-determining regions of the antigen, in Sp pathogenesis.
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PMID:HLA-B27 subtypes in the spondarthropathies. 842 88

In clinical rheumatology, the diagnosis of Chlamydia reactive arthritis is difficult because an incomplete form of the disease can closely resemble an undifferentiated seronegative mono/oligoarthritis. We investigated whether measuring specific isotypes of anti-Chlamydia antibodies in serum can improve the diagnosis, by comparing such antibody concentrations in the serum of patients with well-defined disease, i.e. Chlamydia trachomatis sexually acquired reactive arthritis (CT-SARA), with other arthritides. Antibody levels were determined by enzyme-linked immunosorbent assay (ELISA). When considering two different isotypes and their combination, the best sensitivity (63%) was obtained for IgM and/or IgA results with a specificity of 81%. The patients with CT-SARA and SARA had the highest levels of antibodies of all isotypes tested. It is concluded that, in our experimental conditions, only very high values of specific isotypes could indicate a diagnosis of Chlamydia reactive arthritis.
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PMID:The value of isotype determination of serum antibodies against Chlamydia for the diagnosis of Chlamydia reactive arthritis. 867 May 74

Since the presence of Chlamydia has been shown in synovial fluid (SF) from some patients with Chlamydia reactive arthritis, we investigated whether anti-Chlamydia antibodies present in the joint are derived from the circulation or are locally produced. We compared titres of IgG, IgM and IgA antibodies against Chlamydia, and against a control antigen (tetanus toxoid), by an enzyme-linked immunosorbent assay (ELISA), in paired samples of serum and SF from Chlamydia trachomatis sexually acquired reactive arthritis (CT-SARA) patients and from patients with other forms of arthritis. The ratio of serum/SF IgA anti-Chlamydia antibodies was significantly decreased in CT-SARA patients. It is concluded that, in our experimental conditions, we found evidence for intra-articular production of IgA anti-Chlamydia antibodies.
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PMID:Synovial fluid and serum antibodies against Chlamydia in different forms of arthritis: intra-articular IgA production in Chlamydia sexually acquired reactive arthritis. 867 May 75

Genome-wide gene expression was comparatively investigated in early-passage rheumatoid arthritis (RA) and osteoarthritis (OA) synovial fibroblasts (SFBs; n = 6 each) using oligonucleotide microarrays; mRNA/protein data were validated by quantitative PCR (qPCR) and western blotting and immunohistochemistry, respectively. Gene set enrichment analysis (GSEA) of the microarray data suggested constitutive upregulation of components of the transforming growth factor (TGF)-beta pathway in RA SFBs, with 2 hits in the top 30 regulated pathways. The growth factor TGF-beta1, its receptor TGFBR1, the TGF-beta binding proteins LTBP1/2, the TGF-beta-releasing thrombospondin 1 (THBS1), the negative effector SkiL, and the smad-associated molecule SARA were upregulated in RA SFBs compared to OA SFBs, whereas TGF-beta2 was downregulated. Upregulation of TGF-beta1 and THBS1 mRNA (both positively correlated with clinical markers of disease activity/severity) and downregulation of TGF-beta2 mRNA in RA SFBs were confirmed by qPCR. TGFBR1 mRNA (only numerically upregulated in RA SFBs) and SkiL mRNA were not differentially expressed. At the protein level, TGF-beta1 showed a slightly higher expression, and the signal-transducing TGFBR1 and the TGF-beta-activating THBS1 a significantly higher expression in RA SFBs than in OA SFBs. Consistent with the upregulated TGF-beta pathway in RA SFBs, stimulation with TGF-beta1 resulted in a significantly enhanced expression of matrix-metalloproteinase (MMP)-11 mRNA and protein in RA SFBs, but not in OA SFBs. In conclusion, RA SFBs show broad, constitutive alterations of the TGF-beta pathway. The abundance of TGF-beta, in conjunction with an augmented mRNA and/or protein expression of TGF-beta-releasing THBS1 and TGFBR1, suggests a pathogenetic role of TGF-beta-induced effects on SFBs in RA, for example, the augmentation of MMP-mediated matrix degradation/remodeling.
Arthritis Res Ther 2007
PMID:Constitutive upregulation of the transforming growth factor-beta pathway in rheumatoid arthritis synovial fibroblasts. 1759 88