Absence of Galectin-1 accelerates CD8(+) T cell-mediated graft rejection

Aurelie Moreau; Alistair Noble; Kulachelvy Ratnasothy; Jian-Guo Chai; Louise Deltour; Maria-Cristina Cuturi; Elizabeth Simpson; Robert Lechler; Giovanna Lombardi

doi:10.1002/eji.201142325

Absence of Galectin-1 accelerates CD8(+) T cell-mediated graft rejection

Aurelie Moreau, Alistair Noble, Kulachelvy Ratnasothy, Jian-Guo Chai, Louise Deltour, Maria-Cristina Cuturi, Elizabeth Simpson, Robert Lechler, Giovanna Lombardi

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Abstract

Galectin-1 (Gal-1) is a member of a family of endogenous beta-galactose-binding proteins with a role in preventing autoimmune diseases and chronic inflammation. In this study, the involvement of Gal-1 in graft rejection was investigated by using Gal-1-deficient mice (Gal-1-/-). We demonstrate that in the absence of Gal-1, skin grafts are rejected earlier compared with those of WT mice, and that this is due to the role played by CD8+ T cells in graft rejection. The difference in graft survival observed between Gal-1-/- and WT mice was explained by both an increase in the percentage of antigen-specific CD8+ T cells and by preferential secretion of IFN-gamma and IL-17 by CD8+ T cells in Gal-1-/- mice compared with WT mice. This study suggests that endogenous expression of Gal-1 contributes to graft survival. The results obtained from the use of mice deficient in Gal-1 also confirm a key role for CD8+ T cells in graft rejection.

Original language	English
Pages (from-to)	2881-2888
Number of pages	8
Journal	European Journal of Immunology
Volume	42
Issue number	11
Early online date	5 Sept 2012
DOIs	https://doi.org/10.1002/eji.201142325
Publication status	Published - Nov 2012

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title = "Absence of Galectin-1 accelerates CD8(+) T cell-mediated graft rejection",

abstract = "Galectin-1 (Gal-1) is a member of a family of endogenous beta-galactose-binding proteins with a role in preventing autoimmune diseases and chronic inflammation. In this study, the involvement of Gal-1 in graft rejection was investigated by using Gal-1-deficient mice (Gal-1-/-). We demonstrate that in the absence of Gal-1, skin grafts are rejected earlier compared with those of WT mice, and that this is due to the role played by CD8+ T cells in graft rejection. The difference in graft survival observed between Gal-1-/- and WT mice was explained by both an increase in the percentage of antigen-specific CD8+ T cells and by preferential secretion of IFN-gamma and IL-17 by CD8+ T cells in Gal-1-/- mice compared with WT mice. This study suggests that endogenous expression of Gal-1 contributes to graft survival. The results obtained from the use of mice deficient in Gal-1 also confirm a key role for CD8+ T cells in graft rejection.",

author = "Aurelie Moreau and Alistair Noble and Kulachelvy Ratnasothy and Jian-Guo Chai and Louise Deltour and Maria-Cristina Cuturi and Elizabeth Simpson and Robert Lechler and Giovanna Lombardi",

year = "2012",

month = nov,

doi = "10.1002/eji.201142325",

language = "English",

volume = "42",

pages = "2881--2888",

journal = "European Journal of Immunology",

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TY - JOUR

T1 - Absence of Galectin-1 accelerates CD8(+) T cell-mediated graft rejection

AU - Moreau, Aurelie

AU - Noble, Alistair

AU - Ratnasothy, Kulachelvy

AU - Chai, Jian-Guo

AU - Deltour, Louise

AU - Cuturi, Maria-Cristina

AU - Simpson, Elizabeth

AU - Lechler, Robert

AU - Lombardi, Giovanna

PY - 2012/11

Y1 - 2012/11

N2 - Galectin-1 (Gal-1) is a member of a family of endogenous beta-galactose-binding proteins with a role in preventing autoimmune diseases and chronic inflammation. In this study, the involvement of Gal-1 in graft rejection was investigated by using Gal-1-deficient mice (Gal-1-/-). We demonstrate that in the absence of Gal-1, skin grafts are rejected earlier compared with those of WT mice, and that this is due to the role played by CD8+ T cells in graft rejection. The difference in graft survival observed between Gal-1-/- and WT mice was explained by both an increase in the percentage of antigen-specific CD8+ T cells and by preferential secretion of IFN-gamma and IL-17 by CD8+ T cells in Gal-1-/- mice compared with WT mice. This study suggests that endogenous expression of Gal-1 contributes to graft survival. The results obtained from the use of mice deficient in Gal-1 also confirm a key role for CD8+ T cells in graft rejection.

AB - Galectin-1 (Gal-1) is a member of a family of endogenous beta-galactose-binding proteins with a role in preventing autoimmune diseases and chronic inflammation. In this study, the involvement of Gal-1 in graft rejection was investigated by using Gal-1-deficient mice (Gal-1-/-). We demonstrate that in the absence of Gal-1, skin grafts are rejected earlier compared with those of WT mice, and that this is due to the role played by CD8+ T cells in graft rejection. The difference in graft survival observed between Gal-1-/- and WT mice was explained by both an increase in the percentage of antigen-specific CD8+ T cells and by preferential secretion of IFN-gamma and IL-17 by CD8+ T cells in Gal-1-/- mice compared with WT mice. This study suggests that endogenous expression of Gal-1 contributes to graft survival. The results obtained from the use of mice deficient in Gal-1 also confirm a key role for CD8+ T cells in graft rejection.

U2 - 10.1002/eji.201142325

DO - 10.1002/eji.201142325

M3 - Article

SN - 0014-2980

VL - 42

SP - 2881

EP - 2888

JO - European Journal of Immunology

JF - European Journal of Immunology

IS - 11

ER -

Absence of Galectin-1 accelerates CD8(+) T cell-mediated graft rejection

Abstract

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