Abolition of XXXX -immunosuppression in @entity19 lacking the mu-opioid receptor gene.

@entity19 @entity1337 @entity16119 @entity4784 @entity1961 @entity1286 @entity158
Opiates are potent analgesic and addictive compounds. They also act on immune responses, and @entity1286 , the prototypic opiate, has been repeatedly described as an immunosuppressive drug. Pharmacological studies have suggested that the inhibitory action of opiates on immunity is mediated by multiple opioid receptor sites but molecular evidence has remained elusive. Recently, three genes encoding mu- ( @entity16119 ), delta-, and kappa-opioid receptors have been cloned. To investigate whether the mu-opioid receptor is functionally implicated in @entity1286 immunosuppression in vivo, we have examined immune responses of @entity19 with a genetic disruption of the @entity16119 gene. In the absence of drug, there was no difference between wild-type and mutant @entity19 with regard to a large number of immunological endpoints, suggesting that the lack of @entity16119 -encoded protein has little consequence on immune status. Chronic @entity1286 administration induced lymphoid organ atrophy, diminished the ratio of @entity1961 (+)CD8(+) cells in the thymus and strongly reduced natural killer activity in wild-type @entity19 . None of these effects was observed in @entity16119 -deficient @entity19 after @entity1286 treatment. This demonstrates that the @entity16119 gene product represents a major molecular target for @entity1286 action on the immune system. Because our previous studies of @entity16119 -deficient @entity19 have shown that this receptor protein is also responsible for @entity1286 @entity1337 , reward, and physical dependence, the present results imply that @entity16119 -targeted therapeutic drugs that are developed for the treatment of @entity158 or @entity4784 may concomitantly influence immune responses.
