Absence of Galectin-1 accelerates CD8+ T cell-mediated graft rejection
Absence of Galectin-1 accelerates CD8+ T cell-mediated graft rejection
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DOI:
10.1002/eji.201142325
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发表时间:
2012-11-01
影响因子:
5.4
通讯作者:
Lombardi, Giovanna
中科院分区:
文献类型:
--
作者:
Moreau, Aurelie;Noble, Alistair;Lombardi, Giovanna
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.