False positivity of rheumatoid factor and antibodies to citrullinated peptides in systemic lupus erythematosus.docVIP

Available online /supplements/6/S1 Arthritis Research Therapy Vol 6 Suppl 1, 2004 Meeting abstracts 24th European Workshop for Rheumatology Research Berlin, Germany 26–29 February 2004 Received: 16 January 2004 Published: 25 February 2004 These abstracts are online at /supplements/6/S1 ? 2004 BioMed Central Ltd (Print ISSN 1478-6354; Online ISSN 1478-6362) Autoantibodies and autoantigens 1 epitopes are exposed to anti-CII, with possible formation of surface- bound immune complexes (IC). We investigated whether surface- bound CII anti-CII IC can induce cytokine production from mononuclear cells and the mechanisms behind this. Differential antibody recognition of the 349–364aa B-cell epitope of human La/SSB protein and its phosphorylated analogue Methods ELISA plates were coated with native human CII and blocked with human serum albumin, after which sera with varying concentra- tions of anti-CII were added. Serum-free mononuclear cell cultures from healthy blood donors were then added, and after 20 hours cytokine levels in supernatants were measured using ELISA. Parallel wells without cell cultures were developed as anti-CII ELISAs. Sixty-five RA patients and 10 control individuals were investigated cross-section- ally, and 17 patients with anti-CII followed longitudinally for 1–5 years. FcγRII and FcγRIII were blocked with specific antibodies. Cell deple- tion/enrichment studies were performed to define responder cells. High sensitivity CRP measurement was performed with nephelometry. Results Surface-bound IC containing CII induce TNF-α, IL-1β and IL-8 from mononuclear cells via FcγRII. Cytokine production correlated highly with anti-CII levels in the cross-sectional investigation. Five out of the six longitudinally followed patients with highest anti-CII levels also showed parallel changes in anti-CII OD, cytokine induction and CRP. Deple- tion/enrichment studies showed monocytes to be the res