A pivotal role for galectin-1 in fetomaternal tolerance

Nat Med. 2007 Dec;13(12):1450-7. doi: 10.1038/nm1680. Epub 2007 Nov 18.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / metabolism
  • Female
  • Galectin 1 / genetics
  • Galectin 1 / physiology*
  • Gene Expression Regulation, Developmental*
  • Histocompatibility, Maternal-Fetal*
  • Immune Tolerance*
  • Interleukin-2 Receptor alpha Subunit / biosynthesis
  • Mice
  • Mice, Transgenic
  • Polysaccharides / chemistry
  • Pregnancy
  • Pregnancy, Animal
  • T-Lymphocytes, Regulatory / metabolism
  • Transplantation, Homologous


  • Galectin 1
  • Interleukin-2 Receptor alpha Subunit
  • Polysaccharides