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)

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. 1995 Munksgaard