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- Title
Serotonergic 5-HT<sub>1a</sub> Receptors Regulate a Cell Contact-Mediated Interaction between Natural Killer Cells and Monocytes.
- Authors
Hellstrand, K.; Hermodsson, S.
- Abstract
Autologous monocytes irreversibly suppressed Functions of human natural killer (NK) cells including baseline and lymphokine-induced cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC). and interleukin-2 (IL-2)-induced proliferation. The suppression of these NK-cell functions was cell contact-dependent and could be evoked only by purified monocytes, recovered directly from peripheral blood by countercurrent centrifugal elutriation (CCE). The presence of monocytes also induced the disappearance of CD16 and CD56 antigen on CD3 NK cells (CD3 :16+/56+→CD3 /16+ /56 ). By contrast. T-cell proliferation and the expression of CD3 on CD56 T cells were not susceptible to cell contact-mediated suppression by monocytes. The biogenic amine serotonin abrogated monocyte-induced suppression of NK-cell functions as well as down-modulation of CD16;56 NK-cell antigen. Serotonin thus markedly augmented baseline and lymphokine-induced NK-cell cytotoxicity. ADCC. and NK-cell proliferation. and maintained the expression of NK-cell surface antigens in the presence of elutriated monocytes. The effect of serotonin was mediated by 5-HT1A-type serotonin receptors (5-HT1AR) as indicated by mimicry exerted by 5-HT1AR agonists such as 8-OH-DPAT and (+)-ALK. partial antagonism by the 5-HT1AR antagonists pindolol and cyproheptadine. and lack of antagonism by the 5-HT2R antagonist ketanserin or the 5-HT3 R antagonist ondansetron. Our data are suggestive of a cell-to-cell-mediated mechanism by which monocytes down-modulate NK-cell function and phenotype and its serotonergie regulation.
- Subjects
MONOCYTES; KILLER cells; ANTIBODY-dependent cell cytotoxicity; SEROTONIN antagonists; KETANSERIN; BIOLOGY
- Publication
Scandinavian Journal of Immunology, 1993, Vol 37, Issue 1, p7
- ISSN
0300-9475
- Publication type
Article
- DOI
10.1111/j.1365-3083.1993.tb01658.x