Female sex hormones regulate the Th17 immune response to sperm and Candida albicans

被引：28

作者：

Lasarte, S. ^{[1
,2
]}

Elsner, D. ^{[1
,2
]}

Guia-Gonzalez, M. ^{[1
,2
]}

Ramos-Medina, R. ^{[2
,3
]}

Sanchez-Ramon, S. ^{[2
,3
]}

Esponda, P. ^{[4
]}

Munoz-Fernandez, M. A. ^{[1
,2
]}

Relloso, M. ^{[1
,2
]}

机构：

[1] Hosp Gen Univ Gregorio Maranon, Lab InmunoBiol Mol, Madrid 28007, Spain

[2] Inst Invest Sanit Gregorio Maranon, Madrid 28007, Spain

[3] Hosp Gen Univ Gregorio Maranon, Dept Inmunol Clin, Madrid 28007, Spain

[4] CSIC, Ctr Invest Biol, E-28040 Madrid, Spain

来源：

HUMAN REPRODUCTION | 2013年 / 28卷 / 12期

关键词：

estradiol; spermatozoa; Th17; dendritic cells; DENDRITIC CELLS; SEMINAL PLASMA; ANTISPERM ANTIBODIES; CELIAC-DISEASE; PERITONEAL FLUID; DIFFERENTIATION; MATURATION; PROMOTES; SEMEN; PROGESTERONE;

D O I：

10.1093/humrep/det348

中图分类号：

R71 [妇产科学];

学科分类号：

100211 ;

摘要：

What role do female sex hormones play in the antisperm immune response? We found that sperm induce a Th17 immune response and that estradiol down-regulates the antisperm Th17 response by dendritic cells. Estradiol down-regulates the immune response to several pathogens and impairs the triggering of dendritic cell maturation by microbial products. Ex vivo and in vivo murine models of vaginal infection with sperm and Candida albicans were used to study the induction of Th17 and its hormonal regulation. We analyzed the induction of Th17 cytokines and T cells in splenocytes obtained from BALB/c mice challenged with sperm and C. albicans. For the in vivo vaginal infection models, we used ovariectomized mice treated with vehicle, estradiol or progesterone, and we assessed the effect of these hormones on the immune response in the lymph nodes. Th17 cytokines and T cells were induced by sperm antigens in both ex vivo and in vivo experiments. Estrus levels of estradiol down-regulated the Th17 response to sperm and C. albicans in vivo. This study was conducted using murine models; whether or not the results are applicable to humans is not known. Our results describe an adaptive mechanism that reconciles immunity and reproduction and further explains why unregulated Th17 could be linked to infertility and recurrent infections.

引用

页码：3283 / 3291

页数：9

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