Role of Prolactin in the Recovered T-Cell Development of Early Partially Decapitated Chicken Embryo

Although different experimental approaches have suggested certain regulation of the mammalian immune system by the neuroendocrine system, the precise factors involved in the process are largely unknown. In previous reports, we demonstrated important changes in the thymic development of chickens deprived of the major neuroendocrine centers by the removal of embryonic prosencephalon at 33-38 hr of incubation (DCx embryos) (Herradón et al., 1991; Moreno et al., 1995). In these embryos, there was a stopping of T-cell maturation that resulted in an accumulation of the most immature T-cell subsets (CD4(-)CD8(-) cells and CD4(-)CD8(1o) cells) and, accordingly, in decreased numbers of DP (CD4(+)CD8(+)) thymocytes and mature CD3(+)TcRαβ (+) cells, but not CD3(+)TcRγδ lymphocytes. In the present work, we restore the thymic histology as well as the percentage of distinct T-cell subsets of DCx embryos by supplying recombinant chicken prolactin, grafting of embryonic pituitary gland, or making cephalic chick-quail chimeras. The recovery was not, however, whole and the percentage of CD3(+)TcRαβ thymocytes did not reach the normal values observed in 17-day-old control Sham-DCx embryos. The results are discussed on the basis of a key role for prolactin in chicken T-cell maturation. This hormone could regulate the transition of DN (CD4(-)CD8(-)) thymocytes to the DP (CD4(+)CD8(+)) cell compartment through its capacity for inducing IL-2 receptor expression on the former.