Several observations have contributed to the idea that prolactin may be an important regulator of hematopoiesis and immune function in mammals. First, both the prolactin receptor and ligand have been identified in cells of the hematopoietic system (52-56). Second, pharmacological studies in animals and clinical correlations in humans have shown that prolactin alters parameters of hematopoiesis and immune function (57-61). Third, certain cells cultured from hematopoietic lineages respond to prolactin in vitro (62). Fourth, the prolactin receptor and downstream signaling molecules are homolo gous with proteins that mediate the actions of a variety of hematopoietic cytokines (13). Despite these types of evidence, it has remained difficult to reconcile the idea that prolactin is an essential immunoregulatory hormone with the fundamental requirements of its role in reproduction. prolactin is secreted at much higher levels in females than in males, and at highly variable levels at different phases of the reproduction/lactation cycle. Despite the dramatic fluctuations in prolactin secretion in these situations, the hematopoietic and immune systems undergo no dramatic changes in function corresponding to these differences in prolactin secretion. It is possible to invoke any number of possible explanations for this basic contradiction, but there is insufficient evidence to accept any of these explanations at this time.
To determine whether prolactin is required for any aspect of hematopoiesis of immune function the phenotypes of prolactin-knockout and prolactin-R-knockout mice have been analyzed in detail (17,63). In prolactin-knockout mice, we have showed that the primary development of lymphoid, myeloid, and erythroid lineages was unaltered when prolactin-deficient mice were compared with their normal counterparts. Subsequently, we have examined secondary immune responses, and shown similarly that prolactin-knockout mice are normal with respect to immune functions (unpublished data). Similarly, prolactin-R-knockout mice have normal development of immune cells, and normal responses in terms of antibody synthesis, and mitogen- and antigen-induced proliferation, natural killer (NK) cell cytotoxicity, and other measures of innate and acquired immunity (63).
It is conceivable that there is functional redundancy between prolactin and one or more other hormones which regulate the immune system, and that there are compensatory adjustments for the defects provoked by the absence of prolactin. Another way of looking at the actions of prolactin on the immune system is to consider that these effects may not be specific to the immune system. From this perspective, the impact of prolactin on immunity may be part of a broader role of prolactin as a modulator of stress responses (64). Prolactin acting as a systemic integrator of stress responses, rather than a specific regulator of immune function, would be consistent with its role during pregnancy and lactation, which place high demands on all physiological systems.
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