Sympathetic Regulation of T-helper Cell Function

The role of sympathetic neurotransmission in regulation of T-cell function was examined in mice. After in vivo priming with a model protein antigen, hen egg white lysozyme (HEL), the specific proliferative recall response of lymph node cells (LNCs) was examined. The release of endogenous catecholamines by amphetamine (5 mg/kg, 45 min prior to sacrifice) markedly inhibited the proliferative response of LNCs. Combined alpha- and beta-adrenergic blockade (phentolamine, 1.0 mg/kg+propranolol, 2.5 mg/kg) prevented this effect of amphetamine on proliferation. In vitro, the alpha-adrenergic agonist phenylephrine, but not the beta-agonist isoproterenol, inhibited proliferation in a dose-dependent manner, up to 80%. The effect of phenylephrine was blocked by the alpha-adrenoceptor antagonist phentolamine. The effects of catecholamines appear to be mediated at the level of antigen processing/presentation: Amphetamine given prior to sacrifice inhibited interleukin 2 production when irradiated spleen cells were used to present HEL and HEL-related peptides to HEL-specific T-cell hybridomas. In summary, the sympathetic nervous system seems to inhibit antigen processing/presentation and, indirectly, T-helper responses.