Author: ["Sandra M Blois","Juan M Ilarregui","Mareike Tometten","Mariana Garcia","Arif S Orsal","Rosalia Cordo-Russo","Marta A Toscano","Germán A Bianco","Peter Kobelt","Bori Handjiski","Irene Tirado","Udo R Markert","Burghard F Klapp","Francoise Poirier","Julia Szekeres-Bartho","Gabriel A Rabinovich","Petra C Arck"]
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Abstract
A successful pregnancy requires synchronized adaptation of maternal immune-endocrine mechanisms to the fetus. Here we show that galectin-1 (Gal-1), an immunoregulatory glycan-binding protein, has a pivotal role in conferring fetomaternal tolerance. Consistently with a marked decrease in Gal-1 expression during failing pregnancies, Gal-1–deficient (Lgals1−/−) mice showed higher rates of fetal loss compared to wild-type mice in allogeneic matings, whereas fetal survival was unaffected in syngeneic matings. Treatment with recombinant Gal-1 prevented fetal loss and restored tolerance through multiple mechanisms, including the induction of tolerogenic dendritic cells, which in turn promoted the expansion of interleukin-10 (IL-10)–secreting regulatory T cells in vivo. Accordingly, Gal-1's protective effects were abrogated in mice depleted of regulatory T cells or deficient in IL-10. In addition, we provide evidence for synergy between Gal-1 and progesterone in the maintenance of pregnancy. Thus, Gal-1 is a pivotal regulator of fetomaternal tolerance that has potential therapeutic implications in threatened pregnancies.Cite this article
Blois, S., Ilarregui, J., Tometten, M. et al. A pivotal role for galectin-1 in fetomaternal tolerance. Nat Med 13, 1450–1457 (2007). https://doi.org/10.1038/nm1680 