We have studied the effect of recombinant (r)-Prl on the in vitro-induced MHC-unrestricted cytotoxicity of NK and T cells. A 4-day treatment with r-Prl in serum-free medium enhanced the cytotoxicity of NK cells to the NK-susceptible cell lines K562 and U937, but did not induce de novo NK cytotoxicity in T lymphocytes. By contrast, development of cytotoxicity against the LAK-susceptible cell lines HL60, Jurkat, Daudi and Supt-1 occurred in both NK and T cells. The effect of r-Prl on NK cells was bi-phasic with peaks at 25 ng/ml (1.2 nM), the upper physiological level, and 200 ng/ml (9.6 nM). By contrast, LAK activation of T cells only occurred at the highest r-Prl concentration. In addition to its intrinsic stimulatory activity, r-Prl was also capable of modulating in a dose-dependent manner distinct stages of the IL2-driven LAK/T differentiation pathway. Physiological concentrations of r-Prl interacted with low doses r-IL2 to significantly enhance generation of NK- and T-LAK activities. By contrast, pathological concentrations had opposite effects on generation of optimal LAK response, depending on the kind of LAK progenitor. The T-derived LAK activity was reversibly inhibited at the effector level, while the mature NK-LAK cells were stimulated. These data confirm our previous findings of a co-operative effect of Prl and IL2 on NK cell proliferation and reinforce the view that the signals conveyed by the two factors may be functionally related.
Independent and synergistic effect of interleukin-2 and prolactin on development of T- and NK-derived LAK effectors
MATERA, Lina
1994-01-01
Abstract
We have studied the effect of recombinant (r)-Prl on the in vitro-induced MHC-unrestricted cytotoxicity of NK and T cells. A 4-day treatment with r-Prl in serum-free medium enhanced the cytotoxicity of NK cells to the NK-susceptible cell lines K562 and U937, but did not induce de novo NK cytotoxicity in T lymphocytes. By contrast, development of cytotoxicity against the LAK-susceptible cell lines HL60, Jurkat, Daudi and Supt-1 occurred in both NK and T cells. The effect of r-Prl on NK cells was bi-phasic with peaks at 25 ng/ml (1.2 nM), the upper physiological level, and 200 ng/ml (9.6 nM). By contrast, LAK activation of T cells only occurred at the highest r-Prl concentration. In addition to its intrinsic stimulatory activity, r-Prl was also capable of modulating in a dose-dependent manner distinct stages of the IL2-driven LAK/T differentiation pathway. Physiological concentrations of r-Prl interacted with low doses r-IL2 to significantly enhance generation of NK- and T-LAK activities. By contrast, pathological concentrations had opposite effects on generation of optimal LAK response, depending on the kind of LAK progenitor. The T-derived LAK activity was reversibly inhibited at the effector level, while the mature NK-LAK cells were stimulated. These data confirm our previous findings of a co-operative effect of Prl and IL2 on NK cell proliferation and reinforce the view that the signals conveyed by the two factors may be functionally related.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
