Abstract

Abstract Prolactin (PRL), growth hormone (GH) and placental lactogenic hormones (PL) belong to the growth and lactogenic hormone (GLH) family. These hormones show molecular heterogeneity and the variant hormones differ in their biological activity. GLH receptors are also heterogeneous and have common features with hemopoietic and lymphocyte cytokine receptors. GLH commonly uses signal transducers and activators of transcription (STAT) family transcription factors in the early phase of induction. However, they also act through other signaling systems. Growth hormone and prolactin induce insulin-like growth factor-I (IGF-I) in cells of the immune system and in other tissues and organs. The IGF receptors belong to the transmembrane tyrosine kinase family which signal through phospholipase C-protein kinase C pathway. Placental hormones rather than pituitary GH and PRL support the embryonic development of the immune system. After parturition pituitary GH and PRL in conjunction with IGF-I maintain the bone marrow, thymus and the secondary lymphoid tissue (spleen, lymph noes, mucosal and cutaneous lymphoid system) in a functional state. In the absence of pituitary GH and PRL, the immune system loses rapidly cellularity which is associated with a profound decrease in immunocompetence. Bone marrow function is also decreased. For the normal function of the bone marrow and the immune system, it is sufficient to have normal levels of either pituitary GH or pituitary PRL. Pituitary GLH in conjunction with IGF-I support all immune functions that involve humoral and cell mediated immune responses, innate immune responses and also the internal immunoregulatory pathways. These may lead to the induction of immunological tolerance, anergy and apoptosis induced by cell-to-cell signaling. On this basis, pituitary GLH may be designated as the hormones of immunocompetence. Insulin (INS) is a pleiotropic growth factor which interacts with both GH and IGF-I. Insulin is required for normal immune development and function. In general, INS stimulates immune reactions but inhibitory effects have also been observed. Insulin may be a key regulator of immune function in acute illnesses, which are also characterized by insulin resistance.

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