Present address: Department of Infectious Diseases, Asti General Hospital, Asti, Italy.
Up-modulation of interferon-γ mediates the enhancement of spontanous cytotoxicity in prolactin-activated natural killer cells
Version of Record online: 25 DEC 2001
Volume 98, Issue 3, pages 386–392, November 1999
How to Cite
Matera, L., Contarini, M., Bellone, G., Forno, B. and Biglino, A. (1999), Up-modulation of interferon-γ mediates the enhancement of spontanous cytotoxicity in prolactin-activated natural killer cells. Immunology, 98: 386–392. doi: 10.1046/j.1365-2567.1999.00893.x
- Issue online: 25 DEC 2001
- Version of Record online: 25 DEC 2001
- Received 7 June 1999; accepted 14 July 1999.
Prolactin (PRL) has been shown to participate in lymphocyte activation. In particular, the constitutive natural killer (NK) and the lymphokine-activated killer (LAK) cytotoxicity of CD56+ CD16+ cells is increased by its physiological to supraphysiological concentrations. As PRL has been shown to up-regulate the production of interferon-γ (IFN-γ) by peripheral blood mononuclear cells, we studied its effect on IFN-γ production by NK cells as a possible mechanism of autocrine activation of cytotoxicity. Released and intracellular IFN-γ, as well as IFN-γ mRNA expression, were increased by pituitary and recombinant human PRL, which stimulated optimal NK and LAK cytotoxicity. Treatment with blocking anti-IFN-γ monoclonal antibody (mAb) selectively affected PRL-increased killing of K562 targets, demonstrating that PRL-mediated enhancement of spontaneous cytotoxicity depends, at least in part, on up-regulation of IFN-γ.