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Updated: Sep 20, 2026

Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
Published on: April 15, 2014
Cutting edge: Requirement for growth hormone-releasing hormone in the development of experimental autoimmune
Hideto Ikushima1, Masaharu Kanaoka, Shinichi Kojima
1Research Division, Genomic Research Laboratories, Sumitomo Pharmaceuticals, Osaka, Japan. ikushima@sumitomopharm.co.jp
Abstract:
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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