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Inflammatory arthritis presents in a variety of diseases, from rheumatoid arthritis to hepatitis. Antibodies to autoantigens or to microbial constituents are commonly associated with these conditions. In some cases, the antibodies have diagnostic and prognostic relevance. It cannot as yet be determined definitively that any of them mediate joint damage, although the evidence from animal models indicates that this mechanism is likely. The purpose of this article is to give an overview of the spectrum of antibodies found in a variety of inflammatory arthritides. The relevant animal models are also discussed. [ABSTRACT FROM AUTHOR]

Background In 2007 a genome wide association analyses revealed an additional risk-associated genetic region in rheumatoid arthritis (RA), the tumor necrosis factor receptor-associated factor 1-complement 5 (TRAF1-C5) containing locus on chromosome 9, comprehensive evaluation of the TRAF1 in RA patients remains necessary. Methods Serum was obtained from 79 RA patients and from 38 healthy individuals. Concentrations of TRAF1 were measured by enzyme-linked immune sorbent assay (ELISA). Results We found that the serum concentration of TRAF1 in RA patients was 35.9 ± 51.2 pg/ml, the serum concentration of TRAF1 in healthy controls was 12.5 ± 8.6 pg/ml. The difference between these 2 groups was significant (p = 0.003). Patients with high disease activity had significantly higher TRAF1 concentration in comparison to patients with low and moderate disease activity ( p < 0.05). We also found that the numerical DAS28 had a significant positive correlation with TRAF1 concentration ( r = 0.419, p < 0.001). We found that serum GPI and RF concentrations showed a significant positive correlation with TRAF1 concentrations respectively ( r = 0.767, p < 0.001; r = 0.365, p = 0.001), while CCP concentration showed no significant correlation. Conclusions TRAF1 plays a crucial role in the pathogenesis of autoantibodies and may serve as a serologic inflammatory marker of disease activity in RA patients. [ABSTRACT FROM AUTHOR]