Trophoblast invasion, tissue remodelling and angiogenesis thus occur under a regulated microenvironment that involves active immunosuppressant and tolerogenic circuits such as the selective recruitment of non-cytotoxic NK CD16-CD56bright cells that synthesize angiogenic and growth factors, the induction of regulatory T cells and expansion of natural Tregs, the induction of tolerogenic dendritic cell profile and decidual MBX-102 acid macrophage differentiation to alternative activated phenotypes, among others. Particularly, macrophages represent one of the major leukocyte subsets in decidua throughout pregnancy. During early normal pregnancy, macrophages bear a predominant alternative activation profile contributing to suppressor cytokine and wound healing mediator synthesis. However, macrophages can express a classical Levocabastine hydrochloride inflammatory profile to control the risk of infection by ascending or blood-borne pathogens. In this sense, evidence indicates that macrophage functional profiles are determined by the kind of stimulus and the specific micro-environmental conditions in which cells were differentiated prior to their activation. Fest et al. have previously shown that trophoblast cells secrete chemokines able to recruit maternal macrophages and to modify their secreted cytokine profile. The selective recruitment of different leukocyte populations through a chemokine network also constitutes an additional checkpoint for homeostasis maintenance at the early maternalplacental interface, even in the presence of threatened infection. In fact, chemokines are central to innate and adaptive immunity and they control physiological processes such as wound healing and angiogenesis as well as embryo growth and development. Trophoblast cells actively recruit immune cells through chemokine production and they can also affect immune cell function following the recognition of pathogen associated molecular patterns expressed on bacteria, virus, parasite and fungi through toll like receptors. Stimulation of human trophoblast cells through TLR4 by lipopolysaccharide, TLR2 by peptidoglycan or TLR3 by polyinosinic:polycytidylic acid increases the production of inflammatory chemokines with strong chemottractant effect on CD14+ monocytes to the site of implantation.