Extrathymic Aire-expressing cells support maternal-fetal tolerance.
Eva M Gillis-BuckHaleigh S MillerMarina SirotaStephan J SandersVasilis NtranosMark S AndersonJames M GardnerTippi C MackenziePublished in: Science immunology (2022)
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.
Keyphrases
- mass spectrometry
- induced apoptosis
- single cell
- pregnancy outcomes
- cell cycle arrest
- preterm birth
- endoplasmic reticulum stress
- stem cells
- multiple sclerosis
- oxidative stress
- birth weight
- rna seq
- signaling pathway
- high throughput
- cell proliferation
- working memory
- transcription factor
- mesenchymal stem cells
- cell therapy
- regulatory t cells
- genome wide
- single molecule
- atomic force microscopy