N‐acetylcysteine inhibits the induction of an antigen‐specific antibody response down‐regulating CD40 and CD27 co‐stimulatory molecules

SUMMARY We investigated the effect of N‐acetylcysteine (NAC) on normal human B cell functions. We found that NAC significantly inhibited both the induction of the specific antibody response to the T‐dependent antigen Candida albicans and T‐dependent pokeweed mitogen (PWM)‐induced polyclonal Ig production. NAC did not induce either cell death due to a non‐specific toxicity or apoptosis. The NAC‐induced inhibitory effect might be a functional consequence of: (i) a down‐regulation of the expression on the B cell surface of CD40 and CD27 co‐stimulatory molecules and (ii) a down‐regulation of interleukin (IL‐4) production. In contrast, NAC up‐regulated interferon‐γ (IFN‐γ) production. NAC did not induce any effect on the T cell‐independent B cell polyclonal activation system. These results indicate that NAC down‐regulates T dependent B cell activation and leads to T helper cell type 1 (Th1) polarization.