Previous studies have suggested that prolactin (PRL) may help to regulate T cell development. These observations include showing that PRL and PRL-R mRNA are expressed by thymus, T cells and thymic epithelial cells, and the lack of PRL seems to increase the percentage of immature thymocytes. There also exists a body of correlative or suggestive evidence, such as showing that PRL-R expression coincides with the time that hematopoietic stem cells migrate from the fetal liver to primary lymphoid organs. Finally, the Ames dwarf mouse, which is deficient in PRL, exhibits a variety of immunodeficiencies that can be reversed by PRL therapy. This proposal seeks to determine what role, if any, that PRL plays during T cell development. First, expression of PRL-R by cells from fetal liver and thymocytes recovered at various stages of development will be evaluated. The maturation of T cells in Ames dwarf mice will be studied by following expression of T cell surface maturation markers. Finally, thymocytes exposed to PRL in vitro will be examined for terminal deoxynucleotidyl transferase expression by RT-PCR.
