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

Research output: Contribution to journalArticle

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

Original languageEnglish
Pages (from-to)2881-2888
Number of pages8
JournalEuropean Journal of Immunology
Issue number11
Early online date5 Sep 2012
E-pub ahead of print5 Sep 2012
PublishedNov 2012

King's Authors


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.

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