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Am J Reprod Immunol. 1995 Jan;33(1):134-9.

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).

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Department of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Republic of China.



To test further whether the suppression of the CD3+CD25+ lymphocyte subpopulation by gonadotropin-releasing hormone agonist (GnRH-a) is related to the change in levels of cytokines and soluble interleukin-2 receptor (sIL-2R).


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.


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-1 beta (IL-1 beta), interleukin-2 (IL-2), interleukin-4 (IL-4), interferon-gamma (IFN-gamma), and sIL-2R were not changed.


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.

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