Laboratorio InmunoBiología Molecular, Hospital General Universitario Gregorio Marañón and Instituto de Investigación Sanitaria Gregorio Marañón, Dr. Esquerdo 46, 28007 Madrid, Spain.
Hum Reprod. 2013 Dec;28(12):3283-91. doi: 10.1093/humrep/det348. Epub 2013 Sep 24.
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.
STUDY DESIGN, SIZE, DURATION: 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.
PARTICIPANTS/MATERIALS, SETTING, METHODS: 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.
LIMITATIONS, REASONS FOR CAUTION: 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.
STUDY FUNDING/COMPETING INTEREST(S): This work was supported by research grants from the Instituto de Salud Carlos III (ISCIII) (PI10/00897) and Fundación Mutua Madrileña to M.R. M.R. holds a Miguel Servet contract from the ISCIII (CP08/00228). M.A.M.-F. was supported by (ISCIII) INTRASALUD PI09/02029. We have no conflicts of interest to declare.
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女性性激素在抗精子免疫反应中起什么作用？
我们发现精子诱导了 Th17 免疫反应，而雌二醇通过树突状细胞下调抗精子 Th17 反应。
雌二醇下调了对几种病原体的免疫反应，并损害了微生物产物触发树突状细胞成熟的能力。
研究设计、规模、持续时间：使用阴道感染精子和白色念珠菌的体外和体内鼠模型来研究 Th17 的诱导及其激素调节。
参与者/材料、设置、方法：我们分析了 BALB/c 小鼠受到精子和白色念珠菌挑战后从脾细胞中诱导的 Th17 细胞因子和 T 细胞。对于体内阴道感染模型，我们使用了接受载体、雌二醇或孕酮治疗的卵巢切除小鼠，并评估了这些激素对淋巴结免疫反应的影响。
精子抗原在体外和体内实验中均诱导了 Th17 细胞因子和 T 细胞。发情期雌二醇水平下调了体内对精子和白色念珠菌的 Th17 反应。
局限性、谨慎的原因：本研究使用了鼠模型；这些结果是否适用于人类尚不清楚。
我们的研究结果描述了一种适应性机制，该机制协调了免疫和生殖，并进一步解释了为什么不受调节的 Th17 可能与不孕和反复感染有关。
研究资金/竞争利益：这项工作得到了西班牙卡洛斯三世健康研究所（ISCIII）（PI10/00897）和马德里Mutua Madrileña 基金会的研究资助，M.R. 持有 ISCIII 的 Miguel Servet 合同（CP08/00228）。M.A.M.-F. 得到了（ISCIII）INTRASALUD PI09/02029 的支持。我们没有利益冲突要申报。
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