The British Journal of Rheumatology, Vol 36, 1262-1269, Copyright © 1997 by British Society for Rheumatology
CG Baerwald, M Laufenberg, T Specht, P von Wichert, GR Burmester and A Krause
Previous studies have demonstrated that an alteration of the interaction
between the immune system and the autonomic nervous system may contribute
to the pathogenesis of inflammatory arthritides. To address this issue
further in patients with rheumatoid arthritis (RA), this study aimed at
determining the modulation of beta-adrenergic receptors (beta 2R) on
lymphocyte subsets and its impact on cell reactivity. beta 2R were
determined on CD4+ and CD8+ peripheral blood lymphocytes (PBL) and synovial
fluid lymphocytes (SFL) from RA patients and normal donors. In parallel,
the influence of catecholamines on OKT3- induced T-cell activation was
studied. In patients with RA, beta 2R on SFL were significantly decreased
compared to beta 2R on PBL. Furthermore, a disease activity-correlated
significant decrease of beta 2R on CD8+ PBL was observed. This decrease of
beta 2R was paralleled by a reduced suppressive effect of catecholamines on
OKT3-induced lymphocyte proliferation. Our data give further evidence for
an impaired sympathetic influence on the immune response in RA.
ORIGINAL PAPERS
Impaired sympathetic influence on the immune response in patients with rheumatoid arthritis due to lymphocyte subset-specific modulation of beta 2-adrenergic receptors
Department of Internal Medicine, Philipps-University, Marburg, Germany.
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