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[Modulation of the rate of CD158a+/b+ cells by Th1-and Th2-like cytokines].

AIM
To explore modulation of CD158+ cells in human peripheral blood by Th1-and Th2-like cytokines and provide basic data for inducing immune tolerance and preventing graft-versus-host disease (GVHD) in stem cells transplantation.


METHODS
Peripheral blood mononuclear from healthy adults were cultured with Th1-like cytokines IL-2, IFN-gamma and Th2-like cytokines IL-4, IL-6 for 72 hours, rates of CD3+, CD4+, CD8+ cells, CD16+ CD56+ cells and CD158a+/b+ cells were analyzed by FACS.


RESULTS
(1) The effects of cytokines on CD3+, CD4+, CD8+ and CD16+ CD56+ cells: the rates of above cells were greatly increased after being treated with IL-2 or IFN-gamma(P< 0.05), but efficacy of IL-2 was higher than that of IFN-gamma(P< 0.05). The rates of above cells in IL-2+IFN-gamma treated cells were higher than that in IL-2 or IFN-gamma treated alone. The rates of above cells were greatly decreased after being treated with IL-4+IL-6(P< 0.05), but efficacy of combination of IL-2+IL-4 was higher than that of IL-4 alone, lower than that of IL-2 alone (P< 0.05). (2) The effects of cytokines on CD158a+/b+ cells: the rates of CD158a+/b+ cells in total mononuclear and in CD3+, CD4+, CD8+ and CD16+ CD56+ cells were significantly raised after being treated with IL-2 (P< 0.01), but had no significance changes after being treated with IFN-gamma. The rates of CD158a+/b+ cells were decreased after being treated with IL-4+IL-6, whereas increased after being treated with IL-2+IFN-gamma(P< 0.05), but efficacy of being treated with IL-2+IL-4 was lower than that with IL-2(P< 0.05).


CONCLUSION
IL-2 plays an important role in the regulation of CD158a/b expression or proliferation of CD158a+/b+ cells. It may involve in controlling NK cells and T cells activity via expression of regulating these molecules or stimulating proliferating of CD158a+/b+ cells. IL-4 and IL-6 have a slight ability to decrease the rates of CD158a+/b+ cells and IL-4 can partially reverse the effect of IL-2 on CD158a+/b+ cells.