Impaired sympathetic influence on the immune response in patients with rheumatoid arthritis due to lymphocyte subset-specific modulation of beta 2-adrenergic receptors.

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.