A primate subfamily of galectins expressed at the maternal-fetal interface that promote immune cell death

Nandor Gabor Than, Roberto Romero, Morris Goodman, Amy Weckle, Jun Xing, Zhong Dong, Yi Xu, Federica Tarquini, Andras Szilagyi, Peter Gal, Zhuocheng Hou, Adi L. Tarca, Jai Kim Chong, Jung Sun Kim, Saied Haidarian, Monica Uddin, Hans Bohn, Kurt Benirschke, Joaquin Santolaya-Forgas, Lawrence I. GrossmanOffer Erez, Sonia S. Hassan, Peter Zavodszky, Zoltan Papp, Derek E. Wildman

Research output: Contribution to journalArticlepeer-review


Galectins are proteins that regulate immune responses through the recognition of cell-surface glycans. We present evidence that 16 human galectin genes are expressed at the maternal-fetal interface and demonstrate that a cluster of 5 galectin genes on human chromosome 19 emerged during primate evolution as a result of duplication and rearrangement of genes and pseudogenes via a birth and death process primarily mediated by transposable long interspersed nuclear elements (LINEs). Genes in the cluster are found only in anthropoids, a group of primate species that differ from their strepsirrhine counterparts by having relatively large brains and long gestations. Three of the human cluster genes (LGALS13, -14, and -16) were found to be placenta-specific. Homology modeling revealed conserved three-dimensional structures of galectins in the human cluster; however, analyses of 24 newly derived and 69 publicly available sequences in 10 anthropoid species indicate functional diversification by evidence of positive selection and amino acid replacements in carbohydrate-recognition domains. Moreover, we demonstrate altered sugar-binding capacities of 6 recombinant galectins in the cluster. We show that human placenta-specific galectins are predominantly expressed by the syncytiotrophoblast, a primary site of metabolic exchange where, early during pregnancy, the fetus comes in contact with immune cells circulating in maternal blood. Because ex vivo functional assays demonstrate that placenta-specific galectins induce the apoptosis of T lymphocytes, we propose that these galectins reduce the danger of maternal immune attacks on the fetal semiallograft, presumably conferring additional immune tolerance mechanisms and in turn sustaining hemochorial placentation during the long gestation of anthropoid primates.

Original languageEnglish (US)
Pages (from-to)9731-9736
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number24
StatePublished - Jun 16 2009
Externally publishedYes


  • Adaptive evolution
  • Glycocode
  • Maternal-fetal immune tolerance
  • PP13
  • Preeclampsia

ASJC Scopus subject areas

  • General


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