In Vivo CD3+CD25+ Lymphocyte Subpopulation Is Down-regulated Without Increased Serum-Soluble Interleukin-2 Receptor (sIL-2R) by Gonadotropin Releasing Hormone Agonist (GnRH-a)
Article first published online: 9 MAY 2013
American Journal of Reproductive Immunology
Volume 33, Issue 1, pages 134–139, January 1995
How to Cite
Ho, H.-N., Wu, M.-Y., Chen, H.-F., Chao, K.-H., Yang, Y.-S., Huang, S.-C., Lee, T.-Y. and Gill, T. J. (1995), In Vivo CD3+CD25+ Lymphocyte Subpopulation Is Down-regulated Without Increased Serum-Soluble Interleukin-2 Receptor (sIL-2R) by Gonadotropin Releasing Hormone Agonist (GnRH-a). American Journal of Reproductive Immunology, 33: 134–139. doi: 10.1111/j.1600-0897.1995.tb01150.x
- Issue published online: 9 MAY 2013
- Article first published online: 9 MAY 2013
- Accepted August 25, 1994
- Gonadotropin-releasing hormone;
- soluble interleukin-2 receptor
PROBLEM: To test further whether the suppression of the CD3+CD25+ lymphocyte sub-population by gonadotropin-releasing hormone agonist (GnRH-a) is related to the change in levels of cytokines and soluble interleukin-2 receptor (sIL-2R).
METHOD: Twenty-seven infertile patients were enrolled under the long protocol of GnRH-a agonist (buserelin acetate) and superovulation with gonadotropin from our IVF-ET program. Peripheral B cells, NK cells, CD4+ and CD8+ T cells and the expression of CD69, CD25, HLA-DR, and CD71 antigens on the T cells were serially examined by dual-color flow cytometry. Serum levels of cytokines and sIL-2R were measured.
RESULTS: The B cells, NK cells, T cells, CD4+, CD8+ T cells, CD3+DR+, and CD3+CD71+ lymphocyte subpopulations were not changed after the use of GnRH-a. The CD25+ T cell subpopulation was significantly down-regulated, but the CD69+ T cell subpopulation was increased when the GnRH-a was used for approximately 2 wk. The serum levels of interleukin-lp (IL-1β), interleukin-2 (IL-2), interleukin-4 (IL-4), interferon-γ (IFN-γ), and sIL-2R were not changed.
CONCLUSION: The GnRH-a had a transiently suppressive effect on CD25+ T cells, but a stimulatory effect on CD69+ T cells. However, the serum level of cytokines or sIL-2R did not change. These immunological modulations seems to be the result of interaction between GnRH-a and estrogen.