Soft Landing

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Science  19 Oct 2001:
Vol. 294, Issue 5542, pp. 479
DOI: 10.1126/science.294.5542.479a

Successful embryo implantation can be threatened by inflammation at the site where the blastocyst invades the endometrium. This risk is most significant when paternal proteins differ from those of the mother, because this can provoke a response against the embryo from the maternal immune system. Several mechanisms may explain how this is normally suppressed, including expression of ligands or suppressive factors by trophoblast cells that hinder lymphocyte activity.

Makrigiannakis et al. describe how corticotrophin-releasing hormone (CRH) produced by various cell types after implantation might act to dampen T cell responses within the pregnant womb. In culture, CRH increased expression of Fas ligand (Fas-L) on trophoblast-derived cell lines, which in turn induced apoptosis in activated T cells. A CRH receptor antagonist that impeded Fas-L expression was able to prevent T cell death and, when administered to rats, cut the rate of successful implantation and pregnancy by half. This depended on the presence of T cells capable of reacting against paternal proteins, suggesting that hormone induction of Fas-L may offer the developing embryo protection against the unwanted attention of T cells.—SJS

Nature Immunol., 10.1038/ni719.

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