Growth hormone restores glucocorticoid-induced T cell suppression

Growth hormone (GH) is a potent anabolic hormone, and its clinical use has been extended to the improvement of metabolic imbalance in many disease,s i ncluding autoimmune disorders treated with glucocorticoids (GCs). GH has, h owever, a potential action on the immune system, and this might be a demeri t in GH therapy for those diseases. We report here the anti-GC effects of G H on T lymphocytes. Human peripheral T lymphocytes (HPTLs) expressed GH rec eptor mRNA. GH stimulated tyrosine phosphorylation of cellular proteins, in cluding JAK2 and STAT5b in HPTLs. GH and IGF-I alleviated dexamethasone (De x)-induced suppression of [H-3] thymidine incorporation into HPTLs. GH alle viated Dex-induced apoptosis in CD4(+) (positive) HPTLs. GH increased Bcl-2 expression in CD4(+) HPTLs but not in CD8(+) HPTLs. In vivo, GH raised the CD4/8 ratio of T lymphocytes in rats chronically administered with Dex. Th ese findings indicate that GH may inhibit GC-induced apoptosis predominantl y in CD4(+) T lymphocytes and present important implications of GH therapy, especially for autoimmune disorders treated with GCs.