| First Author | Blois SM | Year | 2007 |
| Journal | Nat Med | Volume | 13 |
| Issue | 12 | Pages | 1450-7 |
| PubMed ID | 18026113 | Mgi Jnum | J:130208 |
| Mgi Id | MGI:3771249 | Doi | 10.1038/nm1680 |
| Citation | Blois SM, et al. (2007) A pivotal role for galectin-1 in fetomaternal tolerance. Nat Med 13(12):1450-7 |
| abstractText | 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. |
