Neuroimmunomodulatory interactions of @entity1063 and XXXX .

@entity1 @entity35 @entity6115 @entity1200 @entity74 @entity750 @entity1154 @entity2922 @entity1063 @entity221 @entity130
@entity1154 neuroleptics alter rodents responses to immunization, suggesting that @entity1063 (NE) and @entity750 ( @entity750 ) are neuroimmunomodulatory in these animals. Although endocrine factors participate in their mechanism(s) of action, recent studies suggest that NE and 5HT also interact more directly with immunocompetent cells. This review provides an overview of evidence for a direct regulatory link between the nervous and immune systems and further speculates on the process by which NE and 5HT realize in part, their neuroimmunomodulatory potential. Anatomical data show that noradrenergic fibers of the sympathetic nervous system innervate lymphoid organs providing a channel of communication between neurons and lymphocytes. Presumably neural signals transmitted by NE are received by platelets that in turn, transduce them via 5HT into immunomodulatory messages. It is proposed that NE alters the capacity of platelets to sequester and/or catabolize 5HT, thus regulating its physiologically active pool in the plasma. Macrophages possess a 5HT uptake system, the kinetic properties of which make them sensitive to changes in plasma levels of the @entity6115 . Thus, through its ability to regulate plasma levels of 5HT, an immunosuppressive @entity6115 with access to macrophages, the nervous system can influence cells involved in antigen recognition. Support for this hypothetical immunomodulatory mechanism is gleaned from clinical and experimental studies. For example, individuals suffering emotional @entity130 are more susceptible than others to developing @entity221 . It is of interest that platelet 5HT pharmacodynamics are often abnormal in @entity1 with @entity74 characterized by @entity2922 deficits. Similar platelet changes have been achieved experimentally by treating @entity35 with @entity2922 antimetabolites. Additional support for the hypothesis derives from aging research since ' @entity1154 imbalance' and @entity1200 are co-characteristics of senescence. In aging rodents and @entity1 , central @entity2922 deficits are associated with a decreased platelet affinity for 5HT and an increased plasma content of 5HT. Thus, emotional, spontaneous (age-related), or experimental changes in @entity1154 homeostasis have the potential to increase the risk of disease in affected individuals. Perhaps part of this effect results from endocrine perturbations associated with the @entity130 . However, a direct interaction between the nervous and immune systems involving @entity1154 is also possible, and a need for future study of this potentially significant mechanism for neuroimmunomodulation is indicated.
