Implantation of the fertilized egg depends on the coordinated interplay of
cells and molecules that prepare the uterus for this important event. In
particular, regulatory T cells (Tregs) are key regulators as their ablation
hinders implantation by rendering the uterus hostile for the embryo. In
addition, the adoptive transfer of Tregs can avoid early abortion in mouse
models. However, it is still not defined which mechanisms underlie Treg
function during this early period. Cells of the innate immune system have been
reported to support implantation, in part by promoting angiogenesis. In
particular, uterine mast cells (uMCs) emerge as novel players at the fetal-
maternal interface. Here, we studied whether the positive action of Tregs is
based on the expansion of uMCs and the promotion of angiogenesis. We observed
that abortion-prone mice have insufficient numbers of uMCs that could be
corrected by the adoptive transfer of Tregs. This in turn positively
influenced the remodeling of spiral arteries and placenta development as well
as the levels of soluble fms-like tyrosine kinase 1 (sFlt-1). Our data suggest
an interplay between Tregs and uMCs that is relevant for the changes required
at the feto-maternal interface for the normal development of pregnancy
