title: 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).
abstract: OBJECTIVE
  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).
  
  
  METHODS
  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-1 beta (IL-1 beta), interleukin-2 (IL-2), interleukin-4 (IL-4), interferon-gamma (IFN-gamma), and sIL-2R were not changed.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Republic of China.
authors.forename: H N
authors.initials: HN
authors.lastname: Ho
authors.forename: M Y
authors.initials: MY
authors.lastname: Wu
authors.forename: H F
authors.initials: HF
authors.lastname: Chen
authors.forename: K H
authors.initials: KH
authors.lastname: Chao
authors.forename: Y S
authors.initials: YS
authors.lastname: Yang
authors.forename: S C
authors.initials: SC
authors.lastname: Huang
authors.forename: T Y
authors.initials: TY
authors.lastname: Lee
authors.forename: T J
authors.initials: TJ
authors.lastname: Gill
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D002064:Buserelin / Q000494:pharmacology*; D017252:CD3 Complex / Q000032:analysis*; D016207:Cytokines / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D005307:Fertilization in Vitro; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors*; D006801:Humans; D016130:Immunophenotyping; D007247:Infertility, Female / Q000276:immunology; D037181:Lectins, C-Type; D018655:Lymphocyte Count / Q000187:drug effects*; D010062:Ovulation Induction; D015375:Receptors, Interleukin-2 / Q000032:analysis*; D016176:T-Lymphocyte Subsets / Q000187:drug effects*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D002064:Buserelin; D017252:CD3 Complex; D016207:Cytokines; D004958:Estradiol; D007987:Gonadotropin-Releasing Hormone; D037181:Lectins, C-Type; D015375:Receptors, Interleukin-2; D000099192:CD69 Antigens