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Cutting Edge: Requirement for Growth Hormone-Releasing Hormone in the Development of Experimental Autoimmune Encephalomyelitis
Author(s) -
Hideto Ikushima,
Masaharu Kanaoka,
Shinichi Kojima
Publication year - 2003
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.171.6.2769
Subject(s) - myelin oligodendrocyte glycoprotein , experimental autoimmune encephalomyelitis , endocrinology , encephalomyelitis , biology , autoimmunity , medicine , immune system , hormone , immunology , splenocyte , receptor , neuropeptide , growth hormone–releasing hormone , central nervous system , growth hormone
Growth hormone (GH)-releasing hormone (GHRH) is a neuropeptide that stimulates secretion of GH from the pituitary gland. Although GHRH and its receptor (GHRHR) are expressed in leukocytes, physiological function of GHRH in the immune system remains unclear. To study the influence of GHRH in autoimmunity, susceptibility to experimental autoimmune encephalomyelitis (EAE) was examined in C57BL/6J-Ghrhr(lit/lit) (lit/lit), mice deficient in the GHRHR gene. We found that lit/lit mice were resistant to myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Splenocytes from MOG-immunized lit/lit mice proliferated normally in response to MOG peptide, suggesting that activation of MOG-specific T cells in GHRHR-deficient mice is not impaired. Our data strongly suggest that GHRH plays a crucial role in the development of EAE and may provide the basis for a novel therapeutic approach protecting from autoimmune diseases.

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