Abstract
The pathogenesis of rheumatic diseases is only incompletely understood, and an imbalance of the immune system seems to play a central role. There ist growing evidence that the autonomic nervous system influences the immune response by stimulation and modulation of the β2-adrenergic receptors (β2R) on lymphocytes. Aim of the study: The present study aimed at evaluating the density and equilibrium constants (KD) of β2R on peripheral blood mononuclear cells (PBMC) in patients with chronic rheumatic diseases. Patients and methods: Characteristics of β2R on PBMC were determined in 10 patients with rheumatoid arthritis (RA) with low systemic disease activity (group 1), 11 patients with RA and high systemic disease activity (group 2), 25 patients with different connective tissue diseases (group 3), and 9 healthy donors (group 4) using a radioligand binding assay with 125Iodocyanopindolol. Results: Compared to normal donors (group 4, mean ± sem, 3,960 ± 372 binding sites/cell, bs/c) the density of β2R was significantly decreased in all patient groups (group 1, 2,418 ± 95 bs/c, p<0.01; group 2, 1,850± 134bs/c, p<0.001; group 3, l,360±16bs/c, p<0.001). The number of β2R in patients with RA and high disease activity (group 2) was significantly lower than in RA patients with low systemic disease activity (group 1). In all three patient groups, a significant negative correlation between β2R density and parameters of the systemic disease activity was observed. Nine patients with systemic lupus erythematosus showed a significant negative correlation between β2R density and serum anti-ds-DNA antibody levels (r = -0.57; p<0.01). Conclusion: These results obtained demonstrate the close correlation between the number of β2R on PBMC and the disease activity in patients with rheumatic diseases. However, in the pathogenesis of immunologically mediated diseases the role of β2R stimulation and modulation remains to be clarified.
Published Version
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