Innate immune cells in reproduction

Abstract

Fetomaternal immune tolerance is required to prevent fetal rejection during pregnancy; simultaneously, the maternal immune system must also protect the fetus from harmful endogenous and exogenous antigens, including those associated with viral and bacterial infections. Therefore, a delicate immune balance is critical for the maintenance of a successful pregnancy, while disruption of this balance can induce complications such as implantation failure, miscarriage, preterm birth/labor, preeclampsia and fetal growth restriction. While the adaptive immune system is critical for the development of tolerance, this review summarizes evidence that modulation of the innate immunity is also essential for achieving this delicate balance between tolerance and protection. Canonical cells of the innate immune system, including dendritic cells, macrophages, natural killer cells and invariant natural killer T cells, contribute to the modulation of the immune balance at the fetomaternal interface. The newly identified myeloid-derived suppressor cells and innate lymphoid cells also appear important for successful reproduction. Moreover, it is possible that sterile inflammation facilitates complications of pregnancy via the innate immune system. In this review, the characteristic features and functions of innate immune cells in fetomaternal immunity and their contributions to pregnancy complications related to sterile inflammation are discussed. These insights on innate immune system function in reproduction may provide new perspectives for understanding the mechanisms of fetomaternal tolerance and the etiology of pregnancy complications.

PDL1 blockage increases fetal resorption and Tfr cells but does not affect Tfh/Tfr ratio and B-cell maturation during allogeneic pregnancy

“…A successful pregnancy requires extremely sophisticated regulation of uterine microenvironment to guarantee the existence of semi-allogeneic conceptus without immune rejection. Orchestrated balance of immune cells residing at the maternal-fetal interface fundamentally contributes to the immune defense protecting the host from external threats, as well as the maintenance of immune tolerance keeping the fetal from maternal immune attack 1,2 . An in-depth exploration into the unique immunological alterations during pregnancy will partially shed light on the pathogenesis of pregnancy-related complications such as spontaneous abortion and preterm delivery, and provide better strategies to improve perinatal outcomes and offspring's health 3,4 .…”

A new function of immunity‐related gene Zn72D in male fertility of Drosophila melanogaster

“…Currently, it is widely recognized that immune defense and reproduction are closely related in a diversity of animals (Ahmed, Stanley, & Kim, ; Negishi, Takahashi, Kuwabara, & Takeshita, ; Schwenke, Lazzaro, & Wolfner, ). One of the mechanisms is that some genes have functions in both immunity and reproduction.…”

From Cancer to Rejuvenation: Incomplete Regeneration as the Missing Link (Part II: Rejuvenation circle)

“…The immunoprivilege provided by trophoblast and deciduas [ 21 ], and the transformation of immune surveillance effectors (T cells, Natural Killer [NK] cells, T helper [Th] 1 cells, M1 macrophages, dendritic cells [DC]) at the mother–fetus interface into regulatory subtypes (T regulatory cells [reg], NK reg, Th2, M2 reg macrophages, DC reg), protects the embryo not only from rejection but also from becoming a tumor. For example, maternal uterine NK reg (as well as the rest of the regulatory subtypes) contributes to the implantation of the embryo by invading a trophoblast consisting of nondividing cells, placentation, spiral artery remodeling and active immunotolerance [ 22 , 23 ]. An important role in these processes belongs to trophoblast cells expressing human leukocyte antigen HLA-G and HLA-E isotypes of the major histocompatibility complex [ 24 , 25 ].…”