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Cooperation of Pituitary Hormone Prolactin with Interleukin‐2 and Interleukin‐12 on Production of Interferon‐γ by Natural Killer and T Cells
Author(s) -
MATERA LINA,
MORI MARCELLA
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb05415.x
Subject(s) - prolactin , interleukin 12 , cytokine , immune system , biology , interleukin 21 , interleukin 15 , endocrinology , t cell , chemistry , hormone , medicine , interleukin , immunology , cytotoxic t cell , in vitro , biochemistry
A bstract : The pituitary hormone prolactin (PRL) is also produced by cells of the immune system and participates in early and late T cell activating events. We have previously shown a modulatory role of PRL during maturation of dendritic cells (DC). Production of IL‐12 by T cell receptor (TCR)‐activated DC is necessary for T cells to acquire the Th1 cytokine (i.e., IFN‐γ secreting) profile, which is associated with activation of cellular response. In a separate work, PRL has been shown to increase IFN‐γ synthesis by natural killer (NK) cells. We have extended that study by exploring the ability of PRL to induce IFN‐γ production by T and NK cells in the presence of the specific stimuli IL‐12 and IL‐2. The individual effect of PRL, IL‐12, and IL‐2 was specific for NK cells, and IL‐2 and IL‐12 were much more efficient than PRL. Cooperation of IL‐2 and PRL was observed on NK cells. IL‐2‐induced synthesis of IFN‐γ was increased by physiological concentrations of PRL but was unaffected or inhibited by high concentrations. By contrast, optimal enhancement of IL‐12‐induced IFN‐γ release was observed with T cells but not with NK cells. Unexpectedly, interaction between PRL and IL‐12 occurred only at high concentrations of PRL. These data indicate a complex role of PRL in the cytokine network and point to a revaluation of the proposed immunosuppression by stress‐related hyperprolactinemia.