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Up‐modulation of interferon‐γ mediates the enhancement of spontanous cytotoxicity in prolactin‐activated natural killer cells
Author(s) -
Matera L.,
Contarini M.,
Bellone G.,
Forno B.,
Biglino A.
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00893.x
Subject(s) - cytotoxicity , lymphokine activated killer cell , interferon gamma , lymphokine , biology , natural killer cell , cd16 , lymphocyte , prolactin , interleukin 12 , k562 cells , peripheral blood mononuclear cell , interleukin 2 , cytotoxic t cell , chemistry , cytokine , immunology , endocrinology , in vitro , cd3 , immune system , cd8 , hormone , biochemistry , leukemia
Summary 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.