AUTOANTIBODY PATTERNS IN SYNOVIAL-FLUIDS FROM PATIENTS WITH RHEUMATOID-ARTHRITIS OR OTHER ARTHRITIC LESIONS

Citation
H. Lettesjo et al., AUTOANTIBODY PATTERNS IN SYNOVIAL-FLUIDS FROM PATIENTS WITH RHEUMATOID-ARTHRITIS OR OTHER ARTHRITIC LESIONS, Scandinavian journal of immunology, 48(3), 1998, pp. 293-299
Citations number
45
Categorie Soggetti
Immunology
ISSN journal
03009475
Volume
48
Issue
3
Year of publication
1998
Pages
293 - 299
Database
ISI
SICI code
0300-9475(1998)48:3<293:APISFP>2.0.ZU;2-D
Abstract
Patients with rheumatoid arthritis (RA) produce a variety of autoantib odies, not only demonstrable in the circulation, but also locally in t he inflamed joint. We investigated the local production of several aut oantibodies in the synovial fluid (SF) of 24 patients with RA and of 2 6 patients with other arthritic lesions. RA patients had higher titres of immunoglobulin M (IgM) and immunoglobulin G (IgG) rheumatoid facto rs (RFs) and of collagen type TI antibodies in SF, whereas there were no demonstrable differences between groups with regard to antibodies a gainst double-stranded (ds) DNA, Clq or the hapten 2,4,6-trinitrobenze ne sulfonic acid (TNP). No differences were observed for total synovia l levels of IgM or IgG. There was no autoantibody pattern that was typ ical of RA patients, except for the local presence of RF, primarily in seropositive RA patients. Our findings therefore support the notion t hat RF and collagen type II antibodies are induced by immunogenic mate rial present in the local inflamed environment. In the accompanying pa per we studied various synovial fluid cytokines in the same patient gr oups. Here we correlated the level of these cytokines with autoantibod y titres in SF, but no specific cytokine associated with the productio n of RF was found. Hence, we conclude that several different inflammat ory mediators might contribute to the chronic inflammation and autoant ibody production in the joint of RA patients. An inverse correlation w as established between concentrations of tumour necrosis factor-alpha (TNF-alpha) and levels of total IgG.