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

Research output: Contribution to journalArticle

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Abstract

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

Original languageEnglish
Pages (from-to)134-139
Number of pages6
JournalAmerican Journal of Reproductive Immunology
Volume33
Issue number1
DOIs
Publication statusPublished - Jan 1 1995
Externally publishedYes

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T Lymphocyte Differentiation Antigens
CD Antigens
Buserelin
CD3 Antigens
Female Infertility
Immunophenotyping
Ovulation Induction
Interleukin-2 Receptors
Lymphocyte Subsets
Lymphocyte Count
T-Lymphocyte Subsets
Fertilization in Vitro
Gonadotropin-Releasing Hormone
Estradiol
Cytokines
T-Lymphocytes
Serum
Natural Killer Cells
B-Lymphocytes
Superovulation

Keywords

  • CD25
  • CD69
  • cytokine
  • Gonadotropin‐releasing hormone
  • soluble interleukin‐2 receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Reproductive Medicine
  • Obstetrics and Gynaecology

Cite this

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

In: American Journal of Reproductive Immunology, Vol. 33, No. 1, 01.01.1995, p. 134-139.

Research output: Contribution to journalArticle

Ho, Hong‐Nerng ‐N ; Wu, Ming‐Yih ‐Y ; Chen, Hsin‐Fu ‐F ; Chao, Kuang‐Han ‐H ; Yang, Yu‐Shih ‐S ; Huang, Su‐Cheng ‐C ; Lee, Tzu‐Yao ‐Y ; Gill, Thomas J. / 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). In: American Journal of Reproductive Immunology. 1995 ; Vol. 33, No. 1. pp. 134-139.
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abstract = "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",
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AU - Wu, Ming‐Yih ‐Y

AU - Chen, Hsin‐Fu ‐F

AU - Chao, Kuang‐Han ‐H

AU - Yang, Yu‐Shih ‐S

AU - Huang, Su‐Cheng ‐C

AU - Lee, Tzu‐Yao ‐Y

AU - Gill, Thomas J.

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