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)


Department of Obstetrics and Gynecology, National Taiwan University Hospital, No. 7 Chung-Shan South Road, Taipei, Taiwan, 100, Republic of China.


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.