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Growth hormone restores glucocorticoid‐induced T cell suppression
Author(s) -
Dobashi Hiroaki,
Sato Makoto,
Tanaka Terukazu,
Tokuda Michiaki,
Ishida Toshihiko
Publication year - 2001
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.00-0702fje
Subject(s) - glucocorticoid , growth hormone , endocrinology , medicine , hormone , chemistry , biology
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 including autoimmune disorders treated with glucocorticoids (GCs). GH has, however, a potential action on the immune system, and this might be a demerit in GH therapy for those diseases. We report here the anti‐GC effects of GH on T lymphocytes. Human peripheral T lymphocytes (HPTLs) expressed GH receptor mRNA. GH stimulated tyrosine phosphorylation of cellular proteins, including JAK2 and STAT5b in HPTLs. GH and IGF‐I alleviated dexamethasone (Dex)‐induced suppression of [ 3 H]thymidine incorporation into HPTLs. GH alleviated 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. These findings indicate that GH may inhibit GC‐induced apoptosis predominantly in CD4 + T lymphocytes and present important implications of GH therapy, especially for autoimmune disorders treated with GCs.