Host responses to immune stimulation, including antigenic stimulation and inflammation, have been described to involve the central neurotransmission, the hypothalamic-pituitary adrenal (HPA) axis, and the immune system. After antigenic stimulation, it has been hypothesized that the HPA axis is involved in a feedback mechanism which limits lymphocyte expansion linked to the immune response. However, such a stimulation of the HPA axis after immunization is not consistently reported in the literature. In the present experiments, we looked for a possible activation of the HPA axis, as well as for the involvement of the sympathetic nervous system during primary and secondary antibody synthesis and cellular immunity. C3H female mice were immunized with low or high doses of sheep red blood cells which induced delayed-type hypersensitivity (DTH) or antibody synthesis, respectively. Plasma corticosterone levels remained in normal ranges whether the animals developed primary or secondary humoral response or DTH. Splenic norepinephrine (NE) levels were unchanged during cellular immunity. During primary and secondary antibody responses splenic NE levels decreased, but no difference appeared between immunized animals and controls when the splenic NE content was expressed in milligrams per spleen because of a spleen enlargement in immunized animals. From these results, it can be concluded that immune responses, antibody synthesis and cellular immunity, in opposition to inflammation, may be induced without any detectable stimulation of the HPA axis or modification of the NE input in the spleen.(ABSTRACT TRUNCATED AT 250 WORDS)