ISSN:
1365-3083
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Histamine (10-1 to 10-7 M) augmcnled natural killer cell cytotoxicity(NKCC)of human CD16+, non-Tlymphocytes in vitro against the NK-sensitive target cells K562erythroleukaemic, Molt-4 lymphoma, Chang liver cells and against Epstein—Barr virus (EBV)-transformed, NK-insensitive Daudi B-lymphohlastoid target ceils by a mechanism of action involving a prostaglandin- and interleukin 1 (IL-l)-independent accessory function of monoeyles. No evidence for the production of intermediary. NK-enhancing cytokines by hisiamine was obtained, indicating a cell-to-cell mediated interaction between monoeytes and NK cells as a plausible mechanism of action for the NK-augmenting effeci. Monocytes recovered by countercurrent centrifugal elutriation (CCE), but not monocyles recovered by adherence, reconstituted the effect of histamine when added to non-adherent NK cells. The development of NKCC in response to histamine was time-dependent with (i) an induction phase, dependent on the presence of accessory monocytes and ongoing hislamine H2-receptor activation (hulf-maximal response required approximately 30 min treatment of large granular lymphocyte (LGL)-enriched lymphocytes and monoeytes with histamine), and (ii) an effector phase, independent of the presence of monocytes or hislamine receptor activation. Hislamine-activated mononuclear cells (MNC) continued to exert augmented cytotoxicity for at least 8 h after removal of histamine and monocytes. In several experiments, histamine-activated NK-effector cells killed 〉 90% of the target cells at low baseline NKCC. We suggest that histatamine may have a role in non-specific tumour defence by regulating an earlier unrecognized interplay between monocytes and NK cells.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1365-3083.1990.tb02814.x
Permalink
