FIGURE 1.

Hypothetical scenario of MC-impact on pregnancy-related processes: undifferentiated MC-precursors migrate from the periphery into the uterus due to the simultaneous influence of estradiol and progesterone. Their local maturation and differentiation occurs through SCF. Amongst other mediators estradiol and progesterone could bind locally on uMCs that further lead to their activation. The MC-activation results in a simultaneous release of pre-formed and/or de novo synthesized mediators including different tryptases and chymases as well as transforming growth factor-β (TGF-β) and histamine. These mediators could directly or indirectly affect important processes like blastocyst’s implantation, decidualization, placentation, spiral artery remodeling, and later on labor. Trophoblast-derived and/or peripheral TGF-β binds on TGF-β-receptors expressed on the mast cell surface that would be a possible further mechanism for their activation. TGF-β likewise stimulates the recruitment of other MCs from the periphery into the fetal–maternal interface. Here, lymph nodes and spleen could serve as a MC-reservoir in the periphery. Fibroblast- and later on trophoblast-derived connective tissue growth factor (CtGF) is involved in matrix degradation, angiogenesis as well as tissue remodeling.