Elevated plasma levels of arginine have been found to correlate with increased secretion of various hormones, including prolactin and growth hormone from the pituitary, insulin, glucagon, insulin-like growth factor 1 (IGF-1) and adrenal catecholamines (see Barbul, 1996). These hormones, in turn, can affect the functioning of the immune system. While the powerful secretagogue action of arginine is largely unexplained, a direct cholinergic effect, membrane depolarization by this highly cationic molecule and subsequent calcium influx, and the use of NO as an intermediary in cell signalling have all been demonstrated.
Prolactin can play a role in various stages of dendritic-cell maturation and T-helper-1 development. Prolactin induces maturation of dendritic cells from monocytes, by increasing their expression of the antigen-presenting MHC class II molecules and co-stimulatory molecules. The expression of CD40 is also up-regulated by prolactin, the final effect being increased T-cell activation. Prolactin can also stimulate the release of T-helper-1 cytokines by T-cells in the absence of dendritic cells (Matera et al., 2000).
The growth hormone receptor is a member of the haematopoietin/cytokine receptor family and induces tyrosine phosphorylation through the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways. While growth hormone is not an absolute requirement for normal lymphoid and myeloid development, under situations of stress it can potentiate the cytokine responses of human T-cells, improve the antigen-presenting capability of dendritic cells, increase the numbers of haematopoietic progenitor cells in the bone marrow and induce thymic hyperplasia (Murphy and Longo, 2000).
IGF-1 plays an important role in the maturation of lymphocytes in the bone marrow and in their function in the periphery. In rodents, IGF-1 can restore age-related thymic involution and increase lymphocyte number and activity (Clark et al., 1993; Hinton et al., 1995). In addition, the thymotropic effects of growth hormone appear to be mediated through IGF-1.
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