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Publication : Absence of Galectin-1 accelerates CD8⁺ T cell-mediated graft rejection.

First Author  Moreau A Year  2012
Journal  Eur J Immunol Volume  42
Issue  11 Pages  2881-8
PubMed ID  22865279 Mgi Jnum  J:188781
Mgi Id  MGI:5442226 Doi  10.1002/eji.201142325
Citation  Moreau A, et al. (2012) Absence of Galectin-1 accelerates CD8+ T cell-mediated graft rejection. Eur J Immunol 42(11):2881-8
abstractText  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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