Abstract

This chapter summarizes the effect of the LH and reward behavior on the augmentation of cellular immunity. In addition to NK cell population and function, T-cell populations and Th1 functions are modulated centrally by the LH and by reward stimulation. LH does not modulate splenic NK cell activity by increasing NK cell numbers, but rather by increasing NK cell activity. Chronic stimulation of the LH caused significant augmentation of NK cell activity. Rats responding to LH stimulation with feeding showed a slightly greater effect than those responding with a locomotor reaction. The observed effects were anatomically specific. The involvement of the LH in reward phenomena was shown to be associated with NK cell augmentation as well. T-cell and Th1 cell functions are sensitive to stress. However, there are no data that illustrate the correlation of reward center with T cells and with their function. Results strongly suggest that excitation of the LH is linked with reward behavior and that pleasure increases type 1 T-cell functions. Ablation of the LH decreased Th1 activity and augmented Th2 activity. The direction of the effects of LH treatment on T-cell function coincides nicely with the effects on NK cells. It might now be safely said that reward links with increased Th1 activity and that, together with NK cell activity, reward or pleasure plays an important role in anticancer, antiviral, and cellular immunity via T-cell cytokine production.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.