Asymmetrical involvement of the cerebral neocortex on the response to an immunopotentiator, sodium diethyldithiocarbamate.

We have previously shown that the neocortex in mice has a lateralized influence on the immune system. A partial left or bilateral neocortical lesion selectively decreases spleen T-cell numbers and function, natural killer and (NK) activity, but a right neocortical lesion do not affect NK activity, and increases T-cell numbers and T-cell-mediated events. Here we report that the immunopotentiating activity of sodium diethyldithiocarbamate (Imuthiol), a compound that selectively increases T-cell numbers and activities, is dependent on an intact neocortex. The effects of Imuthiol were examined in female C3H/HeJ mice 10 weeks after partial neocortical lesions. In animals with right or bilateral neocortical lesions, Imuthiol failed to increase the percentage of spleen T cells, did not influence the expression of class I MHC antigen on these cells, no longer induced the release in serum of specific T-cell-inducing factors, and failed to enhance T-cell-mediated events. In contrast, in animals with a left neocortical lesion, Imuthiol increased T-cell numbers and activities in a fashion that was comparable to that observed in unlesioned controls, but did not enhance NK activity. It is concluded that Imuthiol may affect immune responsiveness by acting directly on the neocortex and/or by interacting at subcortical levels with signals emitted by the neocortex. Moreover, this study reveals a major hemispheric asymmetry in the response to a drug.