Nicotinic receptors regulate B lymphocyte activation and immune response.
Résumé
The presence of nicotinic acetylcholine receptors (nicotinic receptors) composed of either alpha7 or alpha4 and beta2 subunits is revealed in B lymphocytes by means of radioligand binding assay and Cell ELISA. Mouse B lymphocytes contained 12,200+/-3200 of epibatidine-binding sites and 3130+/-750 of alpha-Bungarotoxin-binding sites per cell. Mice lacking nicotinic receptor subunits alpha4, beta2 or alpha7 had less serum IgG and IgG-producing cells in the spleen, but showed stronger immune response to both protein antigen in vivo and CD40-specific antibody in vitro than wild-type mice. Anti-CD40-stimulated proliferation of B lymphocytes from beta2 knockout, but not wild-type mice was inhibited with nicotine. Our results indicate that signalling through nicotinic receptors affects both the pre-immune state and activation of B lymphocytes in the immune response, possibly via CD40-dependent pathway. This could contribute to immune depression found in tobacco smokers.