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spelling paper:paper_10788956_v13_n12_p1450_Blois2023-06-08T16:05:36Z A pivotal role for galectin-1 in fetomaternal tolerance Ilarregui, Juan Martín Toscano, Marta Alicia galectin 1 animal cell animal experiment article controlled study cytokine release dendritic cell fetoplacental unit fetus wastage immunoregulation in vivo culture mouse nonhuman pregnancy disorder priority journal protein binding protein expression regulatory T lymphocyte Animals CD4-Positive T-Lymphocytes Female Galectin 1 Gene Expression Regulation, Developmental Histocompatibility, Maternal-Fetal Immune Tolerance Interleukin-2 Receptor alpha Subunit Mice Mice, Transgenic Polysaccharides Pregnancy Pregnancy, Animal T-Lymphocytes, Regulatory Transplantation, Homologous Mus 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. © 2007 Nature Publishing Group. Fil:Ilarregui, J.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Toscano, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2007 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10788956_v13_n12_p1450_Blois http://hdl.handle.net/20.500.12110/paper_10788956_v13_n12_p1450_Blois
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic galectin 1
animal cell
animal experiment
article
controlled study
cytokine release
dendritic cell
fetoplacental unit
fetus wastage
immunoregulation
in vivo culture
mouse
nonhuman
pregnancy disorder
priority journal
protein binding
protein expression
regulatory T lymphocyte
Animals
CD4-Positive T-Lymphocytes
Female
Galectin 1
Gene Expression Regulation, Developmental
Histocompatibility, Maternal-Fetal
Immune Tolerance
Interleukin-2 Receptor alpha Subunit
Mice
Mice, Transgenic
Polysaccharides
Pregnancy
Pregnancy, Animal
T-Lymphocytes, Regulatory
Transplantation, Homologous
Mus
spellingShingle galectin 1
animal cell
animal experiment
article
controlled study
cytokine release
dendritic cell
fetoplacental unit
fetus wastage
immunoregulation
in vivo culture
mouse
nonhuman
pregnancy disorder
priority journal
protein binding
protein expression
regulatory T lymphocyte
Animals
CD4-Positive T-Lymphocytes
Female
Galectin 1
Gene Expression Regulation, Developmental
Histocompatibility, Maternal-Fetal
Immune Tolerance
Interleukin-2 Receptor alpha Subunit
Mice
Mice, Transgenic
Polysaccharides
Pregnancy
Pregnancy, Animal
T-Lymphocytes, Regulatory
Transplantation, Homologous
Mus
Ilarregui, Juan Martín
Toscano, Marta Alicia
A pivotal role for galectin-1 in fetomaternal tolerance
topic_facet galectin 1
animal cell
animal experiment
article
controlled study
cytokine release
dendritic cell
fetoplacental unit
fetus wastage
immunoregulation
in vivo culture
mouse
nonhuman
pregnancy disorder
priority journal
protein binding
protein expression
regulatory T lymphocyte
Animals
CD4-Positive T-Lymphocytes
Female
Galectin 1
Gene Expression Regulation, Developmental
Histocompatibility, Maternal-Fetal
Immune Tolerance
Interleukin-2 Receptor alpha Subunit
Mice
Mice, Transgenic
Polysaccharides
Pregnancy
Pregnancy, Animal
T-Lymphocytes, Regulatory
Transplantation, Homologous
Mus
description 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. © 2007 Nature Publishing Group.
author Ilarregui, Juan Martín
Toscano, Marta Alicia
author_facet Ilarregui, Juan Martín
Toscano, Marta Alicia
author_sort Ilarregui, Juan Martín
title A pivotal role for galectin-1 in fetomaternal tolerance
title_short A pivotal role for galectin-1 in fetomaternal tolerance
title_full A pivotal role for galectin-1 in fetomaternal tolerance
title_fullStr A pivotal role for galectin-1 in fetomaternal tolerance
title_full_unstemmed A pivotal role for galectin-1 in fetomaternal tolerance
title_sort pivotal role for galectin-1 in fetomaternal tolerance
publishDate 2007
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10788956_v13_n12_p1450_Blois
http://hdl.handle.net/20.500.12110/paper_10788956_v13_n12_p1450_Blois
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