| Literature DB >> 34272228 |
Eva Gillis-Buck1, Haleigh Miller2,3,4, Marina Sirota3,5, Stephan J Sanders6,7, Vasilis Ntranos2,3,4, Mark S Anderson4,8, James M Gardner9,4, Tippi C MacKenzie9,5,7.
Abstract
Healthy pregnancy requires tolerance to fetal alloantigens as well as syngeneic embryonic and placental antigens. Given the importance of the autoimmune regulator (Aire) gene in self-tolerance, we investigated the role of Aire-expressing cells in maternal-fetal tolerance. We report that maternal ablation of Aire-expressing (Aire +) cells during early mouse pregnancy caused intrauterine growth restriction (IUGR) in both allogeneic and syngeneic pregnancies. This phenotype is immune mediated, as IUGR was rescued in Rag1-deficient mice, and involved a memory response, demonstrated by recurrence of severe IUGR in second pregnancies. Single-cell RNA sequencing demonstrated that Aire + cell depletion in pregnancy results in expansion of activated T cells, particularly T follicular helper cells. Unexpectedly, selective ablation of either Aire-expressing medullary thymic epithelial cells or extrathymic Aire-expressing cells (eTACs) mapped the IUGR phenotype exclusively to eTACs. Thus, we report a previously undescribed mechanism for the maintenance of maternal-fetal immune homeostasis and demonstrate that eTACs protect the conceptus from immune-mediated IUGR.Entities:
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Year: 2021 PMID: 34272228 PMCID: PMC9363019 DOI: 10.1126/sciimmunol.abf1968
Source DB: PubMed Journal: Sci Immunol ISSN: 2470-9468