Altered prolactin response of the lymphocytes of tumor-bearing mice

✍ Scribed by Ratna Biswas; Utpala Chattopadhyay

• Book ID: 102864210
• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: French
• Weight: 648 KB
• Volume: 50
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910500119

✦ Synopsis

Interaction of prolactin and glucocorticoid on thymocytes and splenocytes of normal and tumor-bearing mice with reference to their mitogen-responsive blastogenesis has been studied. Prolactin alone had little or no mitogenic effect on thymocytes and splenocytes of normal mice but it was co-stimulatory, with ConA, in inducing blastogenesis in normal splenocytes. Thymocytes and splenocytes of tumor-bearing mice responded differently to prolactin. Hormone alone inhibited growth of thymocytes but at certain concentrations stimulated splenocytes. When cultured with prolactin and C o d , the thymocytes of tumor hosts responded with increased proliferation compared to that induced by ConA alone. Glucocorticoid suppressed ConA-induced lymphocyte proliferation in both normal and tumor-bearing mice. Prolactin reversed the inhibitory effect of glucocorticoid in normal mice but failed to abrogate inhibition in tumor hosts. Altered responsiveness of lymphocytes of tumor hosts to prolactin was not a function of circulating prolactin, as the serum prolactin level was similar in normal and tumorbearing mice. Prolactin, however, could not reverse estradiolinduced suppression of lymphocyte proliferation. The lactogenic hormone, but not somatogenic hormones, altered the glucocorticoid inhibition of lymphocyte growth.

The role of pituitary hormones in regulating immune response is well established (Dougherty, 1952;Berczi and Nagy, 1987). The pituitary gland secretes prolactin (Prl) and growth hormone (GH) that stimulates the immune system (Comsa et al.