Prolactin induced reversal of glucocorticoid mediated apoptosis of immature cortical thymocytes is abrogated by induction of tumor.

Glucocorticoid (GC) and prolactin (PRL) are the two neuroendocrines that regulate thymocyte differentiation and maintain the immune homeostasis during stress. We found that dexamethasone (Dex), a synthetic GC, induced apoptosis in normal immature cortical thymocytes which remained unaltered in the presence of Elrich's ascitic carcinoma (EAC). PRL protected the normal CD4+ CD8+ cortical thymocytes from Dex-induced apoptosis but failed to alter the effect of Dex in tumor-bearing mice. Dex-treated normal thymocytes became unresponsive to PRL in presence of tumor cell culture supernatant. Low binding affinity of the microsomal membranes of thymocytes to PRL and absence of the mRNA of a particular form of prolactin receptor (PRL-R) suggest the presence of a different PRL-R in CD4+ CD8+ thymocytes of EAC-bearing mice. The induction of tumor may alter the PRL-R that can be correlated with the failure of PRL in rescuing CD4+ CD8+ immature cortical thymocytes from GC induced death.