C. Baerwald et al., BETA(2)-ADRENERGIC RECEPTORS ON PERIPHERA L-BLOOD MONONUCLEAR-CELLS IN PATIENTS WITH RHEUMATIC DISEASES, Aktuelle Rheumatologie, 20(2), 1995, pp. 43-48
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 influence
s the immune response by stimulation and modulation of the beta(2)-adr
energic receptors (beta(2)R) on lymphocytes. Aim of the study: The pre
sent study aimed at evaluating the density and equilibrium constants (
KD) of beta(2)R on peripheral blood mononuclear cells (PBMC) in patien
ts with chronic rheumatic diseases. Patients and methods: Characterist
ics of beta(2)R on PBMC were determined in 10 patients with rheumatoid
arthritis (RA) with low systemic disease activity (group 1), 11 patie
nts with RA and high systemic disease activity (group 2), 25 patients
with different connective tissue diseases (group 3), and 9 healthy don
ors (group 4) using a radioligand binding assay with (125)Iodocyanopin
dolol. Results: Compared to normal donors (group 4, mean+/-sem, 3,960/-372 binding sites/cell, bs/c) the density of beta(2)R was significan
tly decreased in all patient groups (group 1, 2,418+/-95 bs/c, p < 0.0
1; group 2, 1,850+/-134 bs/c, p < 0.001; group 3, 1,360+/-16 bs/c, p <
0.001). The number of beta(2)R in patients with RA and high disease a
ctivity (group 2) was significantly lower than in RA patients with low
systemic disease activity (group 1). In all three patient groups, a s
ignificant negative correlation between beta(2)R density and parameter
s of the systemic disease activity was observed. Nine patients with sy
stemic lupus erythematosus showed a significant negative correlation b
etween beta(2)R 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 beta(2)R on PBMC and the disease act
ivity in patients with rheumatic diseases. However, in the pathogenesi
s of immunologically mediated diseases the role of beta(2)R stimulatio
n and modulation remains to be clarified.