Exp Clin Endocrinol Diabetes 2004; 112(10): 587-594
DOI: 10.1055/s-2004-830404
Article

J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Expression of Gonadotropin-Releasing Hormone Type-I (GnRH-I) and Type-II (GnRH-II) in Human Peripheral Blood Mononuclear Cells (PMBCs) and Regulation of B-Lymphoblastoid Cell Proliferation by GnRH-I and GnRH-II

F. Tanriverdi1 , 2 , D. Gonzalez-Martinez2 , L. F. G. Silveira2 , Y. Hu2 , G. S. Maccoll2 , P. Travers3 , P. M. G. Bouloux2
  • 1Department of Endocrinology, Erciyes University Medical School, Talasyolu, Kayseri, Turkey
  • 2Department of Medicine, Neuroendocrine Unit, Royal Free and University College Medical School, London, UK
  • 3Immunology Unit, Royal Free and University College Medical School, London, UK
Further Information

Publication History

Received: October 23, 2003 First decision: December 15, 2003

Accepted: May 3, 2004

Publication Date:
02 December 2004 (online)

Abstract

GnRH-I and its receptor (GnRHR-I) have previously been demonstrated and shown to be biologically active in the immune system, notably within T cells. Recently however a second form of GnRH (GnRH-II) has been described in the human. The function of both these neuropeptides in B lymphocytes has not previously been explored. The present study investigates GnRH-I and GnRH-II expression in human peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), as well as their action in regulating B-LCL proliferation in the presence and absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a normal control. RT-PCR and immunocytochemistry identified locally produced GnRH-I and GnRH-II in all cell groups. Treatment of normal B-LCLs with GnRH-I (10-9 M and 10-5 M) or with interleukin-2 (IL-2) (50 IU/ml) resulted in a significant increase in cell proliferation compared with the untreated control. IL-2 and GnRH-I (10-7 M, 10-6 M, 10-5 M) induced greater proliferation in normal B-LCLs than IL-2 treatment alone. No significant proliferation occurred in GnRHR-I defective B-LCLs, in response to either GnRH-I (10-9 and 10-5 M) or IL-2 treatment, nor to IL-2 and GnRH-I (10-10 to 10-5 M) co-treatment when compared to controls. Co-incubation of IL-2 and IL-2 + GnRH 10-5 M with a GnRH antagonist (Cetrorelix; 10-6 M) significantly attenuated the proliferation in normal B-LCLs. GnRH-II did not affect proliferation of normal B-LCLs alone, and did not alter the proliferative response to IL-2. Further investigation is required to clarify the physiological relevance of local GnRH-I/GnRH-II in immune system responsiveness.

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Fatih Tanriverdi

Department of Endocrinology
Erciyes University Medical School

38039 Talasyolu, Kayseri

Turkey

Phone: + 903522338323

Fax: + 90 35 24 37 58 07

Email: fatihtan@erciyes.edu.tr

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