LAUSR

only during embronic development (eg, carcinoembryonic antigen). The fetus is not completely physically isolated from the maternal immune system, and there is evidence for the development of an adaptive immune response during pregnancy. In fact, pregnancy is a known sensitizer and causative factor in the development of anti-HLA antibodies that can be detrimental in transplantation. Mechanisms responsible for suppression of antifetal responses that might otherwise result in an aborted pregnancy are not simply due to the physical fetal-maternal placental barrier, but due to active cellular mechanisms that may be discerned in mixed lymphocyte reactions. FOXP3+ regulatory T cells (Treg) are at least partly responsible for maintaining maternal-fetal tolerance and are found in high numbers in decidual tissues. In some experimental models, depletion of Treg results in pregnancy resorption, highlighting the importance of this cell population in maintaining allogeneic pregnancies. The relevance of the various Treg subtypes that are present, however, is currently lacking. Salvany-Celades et al present an in-depth characterization of human decidual Treg types. Using flow cytometry, 3 separate populations were investigated: CD25FOXP3, PD1IL-10, and TIGITFOXP3. On isolation, all 3 populations were found to suppress both the proliferation and cytokine production of both CD4 and CD8 effector T cells in vitro. Interestingly, extra-villous trophoblasts as well as decidual macrophages isolated from the firsttrimester placental tissue were able to increase the proportion of FOXP3 Treg when cocultured with peripheral blood CD4 T cells. Extra-villous trophoblasts (but not macrophages) increased PD1 Treg with neither population having an effect on TIGIT Treg. Overall, this study provides additional clarity to the fascinating tolerogenic mechanisms that are active during pregnancy in addition to the powerful role Treg play in maintaining immune homeostasis when needed. Understanding how these cells function in “nature’s transplant” provides opportunities to harness their suppressive mechanisms therapeutically in the development of tolerogenic therapies for transplantation.