High anti-collagen type-II antibody levels and induction of proinflammatory cytokines by anti-collagen antibody-containing immune complexes in vitro characterise a distinct rheumatoid arthritis phenotype associated with acute inflammation at the time of disease onset. Issue 4 (13th October 2006)

• Record Type: Journal Article
• Authors: Mullazehi, Mohammed; Mathsson, Linda; Lampa, Jon; Rönnelid, Johan
• Is Part Of: Annals of the rheumatic diseases. Volume 66:Issue 4(2007)
• Page Start: 537
• Page End: 541
• Publication Date: 2006-10-13
• Subjects: AU, arbitrary unit -- BSA, bovine serum albumin -- CII, collagen type II -- CRP, C reactive protein -- DAS, disease activity score -- DMARD, disease-modifying antirheumatic drug -- ESR, erythrocyte sedimentation rate -- IC, immune complex -- IL, interleukin -- OD, optical density -- PBMC, peripheral blood mononuclear cell -- PBS, phosphate-buffered saline -- RA, rheumatoid arthritis -- RF, rheumatoid factor -- TNF, tumour necrosis factor; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/ard.2006.064782
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Objective: To investigate whether the cytokine-inducing properties of surface-bound collagen type II (CII)-containing immune complexes (IC), which were reported earlier, have any clinical impact. Methods: Anti-CII serology was analysed in 274 patients with early rheumatoid arthritis (RA). Patients with increased levels of anti-CII were followed serially for 1–5 years with regard to anti-CII IC-induced levels of tumour necrosis factor (TNF)α, interleukin (IL)1β and IL8. Levels of antibodies and IC-induced cytokines were compared with clinical indices over 5 years of follow-up. Results: 5/100 healthy controls and 24/274 (8.8%) patients with RA exhibited increased levels (>29 arbitrary units (AU)/ml) of anti-native CII antibodies, a non-significant difference. 9/274 (3.3%) patients with RA and no controls comprised a discrete group with high anti-CII levels >450 AU/ml. These high anti-CII level sera were associated with induction of pro-inflammatory cytokines by anti-CII-containing IC formed in vitro. 8/9 patients with high baseline anti-CII levels exhibited a parallel decline in antibody levels, IC-induced cytokines, C reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Anti-CII-positive patients had significantly increased levels of CRP and ESR at baseline, but not later during the follow-up. Conclusions: Anti-native CII-positive patients with RA have a distinct clinical phenotype characterised by an early acute phase response that might be driven by anti-CII-containing IC in joint cartilage.