In vivo and in vitro data combined show that prolactin (PRL) can mimic or interact with known lymphocyte cytokines and that these, in turn, can regulate PRL synthesis at the site of immune response. In contrast, pituitary PRL is under the control of both immune system products (non-cognitive stimuli) and signals to the CNS (cognitive stimuli). The role of PRL as a cytokine and as an endocrine hormone is discussed. In particular, assignment of PRL to the T helper 1 phenotype is proposed, based on its ability to enhance NK cell function, activate the interferon-regulated factor (IRF-1) transcription factor and to interact with or generate IL-2 and IFN gamma. Since hyperprolactinemia and hypoprolactinemia are both immunosuppressive, physiological levels of circulating PRL must be necessary to maintain normal immunocompetence. Moderate increases in PRL during immune stimulation of the hypothalamic-pituitary axis may counteract glucocorticoid inhibition, whereas inappropriate prolongation of PRL synthesis could lead to autoimmune diseases. Increased release of PRL by the pituitary during stress may inhibit NK cell antitumor cytotoxicity. The variety of PRL isotypes, the existence of multiple receptor subunits, and the complexity of their intracellular signaling may explain the specificity of PRL action on different target cells.
Action of pituitary and lymphocyte prolactin.
MATERA, Lina
1997-01-01
Abstract
In vivo and in vitro data combined show that prolactin (PRL) can mimic or interact with known lymphocyte cytokines and that these, in turn, can regulate PRL synthesis at the site of immune response. In contrast, pituitary PRL is under the control of both immune system products (non-cognitive stimuli) and signals to the CNS (cognitive stimuli). The role of PRL as a cytokine and as an endocrine hormone is discussed. In particular, assignment of PRL to the T helper 1 phenotype is proposed, based on its ability to enhance NK cell function, activate the interferon-regulated factor (IRF-1) transcription factor and to interact with or generate IL-2 and IFN gamma. Since hyperprolactinemia and hypoprolactinemia are both immunosuppressive, physiological levels of circulating PRL must be necessary to maintain normal immunocompetence. Moderate increases in PRL during immune stimulation of the hypothalamic-pituitary axis may counteract glucocorticoid inhibition, whereas inappropriate prolongation of PRL synthesis could lead to autoimmune diseases. Increased release of PRL by the pituitary during stress may inhibit NK cell antitumor cytotoxicity. The variety of PRL isotypes, the existence of multiple receptor subunits, and the complexity of their intracellular signaling may explain the specificity of PRL action on different target cells.
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