Article

Uterine NK cells: Active regulators at the maternal-fetal interface

The Journal of clinical investigation (Impact Factor: 13.22). 05/2014; 124(5):1872-1879. DOI: 10.1172/JCI68107
Source: PubMed

ABSTRACT

Pregnancy presents an immunological conundrum because two genetically different individuals coexist. The maternal lymphocytes at the uterine maternal-fetal interface that can recognize mismatched placental cells are T cells and abundant distinctive uterine NK (uNK) cells. Multiple mechanisms exist that avoid damaging T cell responses to the fetus, whereas activation of uNK cells is probably physiological. Indeed, genetic epidemiological data suggest that the variability of NK cell receptors and their MHC ligands define pregnancy success; however, exactly how uNK cells function in normal and pathological pregnancy is still unclear, and any therapies aimed at suppressing NK cells must be viewed with caution. Allorecognition of fetal placental cells by uNK cells is emerging as the key maternal-fetal immune mechanism that regulates placentation.

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Available from: Francesco Colucci, Dec 11, 2014
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    • "The selective expression of p110d in leukocytes has made it an attractive pharmacological target to treat hematological malignancies and reduce unwanted immune responses in the context Cell Reports 13, 2817–2828, December 29, 2015 ª2015 The Authors 2817 of autoimmunity and allergy (Rodon et al., 2013). Maternal immune adaptations during pregnancy are instrumental for the development of the growing fetus (Erlebacher, 2013; Moffett and Colucci, 2014). We used transgenic knockin mice carrying a kinase-dead point mutation in the gene coding for p110d (d D910A ) as a genetic model for inactivation of the p110d pathway in order to investigate the effects of unbalanced maternal immune responses during gestation. "
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