No change in plasma @entity2819 and splenic @entity1063 during humoral and cellular immune responses to @entity742 erythrocytes in C3H XXXX .

@entity32 @entity742 @entity19 @entity2819 @entity2339 @entity56 @entity1063
Host responses to immune stimulation, including antigenic stimulation and @entity32 , have been described to involve the central neurotransmission, the @entity2339 , and the immune system. After antigenic stimulation, it has been hypothesized that the @entity2339 is involved in a feedback mechanism which limits lymphocyte expansion linked to the immune response. However, such a stimulation of the @entity2339 after immunization is not consistently reported in the literature. In the present experiments, we looked for a possible activation of the @entity2339 , as well as for the involvement of the sympathetic nervous system during primary and secondary antibody synthesis and cellular immunity. C3H female @entity19 were immunized with low or high doses of @entity742 red blood cells which induced @entity56 ( @entity56 ) or antibody synthesis, respectively. Plasma @entity2819 levels remained in normal ranges whether the animals developed primary or secondary humoral response or @entity56 . Splenic @entity1063 (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 @entity32 , may be induced without any detectable stimulation of the @entity2339 or modification of the NE input in the spleen.(ABSTRACT TRUNCATED AT 250 WORDS)
