Immune interactions at the maternal-fetal interface.
Models of murine allogeneic pregnancy have established that maternal T cells recognize fetal alloantigens and are normally suppressed or deleted. While the precise cellular interactions and mechanisms involved in maternal lymphocyte tolerance are not yet clear, the identity of some of the critical factors are beginning to be uncovered. Signals that have been shown in mice to have an obligatory role in immunological survival of the semiallogeneic fetus include, but are probably not limited to, indoleamine-2,3-dioxygenase and the newly discovered B7 family protein, B7-H1. Whether these proteins have intersecting functions is unknown, but it is possible that both are involved in the control of maternal T regulatory cells, which are also strictly required for successful allogeneic pregnancy in mice. Additional factors that are involved include trophoblast and/or maternally derived FasL, and in humans, class Ib HLA molecules. The potency of these mechanisms in protecting the fetal allograft is underscored by the scarcity of knockout and transgenic models in which pregnancy is immunologically compromised. Here, the current understanding of mechanisms of specific suppression of maternal lymphocytes is reviewed.[1]References
- Immune interactions at the maternal-fetal interface. Petroff, M.G. J. Reprod. Immunol. (2005) [Pubmed]
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