@article {10.3844/ajisp.2006.35.39,
article_type = {journal},
title = {Loss of Morphine-induced Suppression of NK Cell activity and T-cell Functions in µ-Opioid Receptor Knockout Mice},
author = {Weber, Richard J. and Gomez-Flores, Ricardo and Sora, Ichiro and Uhl, George R.},
volume = {2},
year = {2006},
month = {Jun},
pages = {35-39},
doi = {10.3844/ajisp.2006.35.39},
url = {https://thescipub.com/abstract/ajisp.2006.35.39},
abstract = {In vivo administration of µ-opioid receptor selective agonists to various species is known to suppress lymphocyte, NK cell, and macrophage functions, in addition to mediate pain relief and euphoria. Using a mouse model in which the µ-opioid receptor gene was disrupted by targeted homologous recombination, we explored the involvement of this receptor in natural killer (NK) cell activity and T lymphocyte function. Following peripheral morphine administration, NK cell activity was not affected in homozygous µ-opioid receptor knockout mice, heterozygous animals marginally responded to the immunosuppressive effects of the drug, while wild-type animals were significantly suppressed. In addition, splenic T-cell proliferative responses to concanavalin A, phytohemaglutinin and an antibody to T-cell receptorabαβ (TCR) plus interleukin-2 were not affected by morphine treatment in µ-opioid receptor knockout homozygous and heterozygous mice, whereas morphine significantly suppressed T-cell proliferation in wild-type mice. Taken together, these results suggest a role of the µ-opioid receptor in immunoregulation.},
journal = {American Journal of Immunology},
publisher = {Science Publications}
}