Serotonin (5-HT) augments NK cell activity (NKCA) in vitro. NKCA is a component of the innate immune response to viral infection and certain tumor cells. Further, 5-HT1a receptor agonists bolster NKCA in vitro. In addition, studies suggest that lymphocytes express 5-HT reuptake transport proteins. In light of these reports, NK cells were treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine and/or the S-HT1a antagonist pindobind to further characterize serotonergic modulation of NKCA. Mononuclear cells, isolated from human blood, were incubated with drug and a standard 51chromium-release assay performed with K562 target cells. A 4 hr cytotoxicity assay was conducted and NKCA quantified as lytic units 5-HT, a 5-HT1a receptor agonist (8-OH-DPAT), and fluoxetine augmented NKCA whereas pindobind suppressed NKCA and abrogated the augmenting effects of fluoxetine. The present results provide further evidence of serotonergic modulation of NKCA through the 5-HT1a receptor and suggest a potentially important role for serotonergic agents such as SSRIs in the clinical regulation of immune function.
|Original language||English (US)|
|Publication status||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology