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)

Hong‐Nerng ‐N Ho, Ming‐Yih ‐Y Wu, Hsin‐Fu ‐F Chen, Kuang‐Han ‐H Chao, Yu‐Shih ‐S Yang, Su‐Cheng ‐C Huang, Tzu‐Yao ‐Y Lee, Thomas J. Gill

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28 引文 斯高帕斯(Scopus)

摘要

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
原文英語
頁(從 - 到)134-139
頁數6
期刊American Journal of Reproductive Immunology
33
發行號1
DOIs
出版狀態已發佈 - 一月 1 1995
對外發佈

ASJC Scopus subject areas

  • 免疫學和過敏
  • 免疫學
  • 生殖醫學
  • 婦產科

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