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Absence of Galectin‐1 accelerates CD8+ T cell‐mediated graft rejection
Authors:Aurélie Moreau  Alistair Noble  Kulachelvy Ratnasothy  Jian‐Guo Chai  Louise Deltour  Maria‐Cristina Cuturi  Elizabeth Simpson  Robert Lechler  Giovanna Lombardi
Affiliation:1. MRC Centre for Transplantation, King's College London, Guy's Hospital, , London, UK;2. MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, King's College London, Guy's Hospital, , London, UK;3. Section of Immunobiology, Division of Immunology and Inflammation, Faculty of Medicine, Imperial College London, , London, UK;4. Institut Jacques Monod, UMR 7592 CNRS, Université Paris Diderot, , Paris, France;5. ITUN/INSERM U643, CHU Hotel‐Dieu, , Nantes, France
Abstract:Galectin‐1 (Gal‐1) is a member of a family of endogenous β‐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‐γ 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.
Keywords:Cytokines  Galectin‐1  Knockout mice  Tc1 CD8+ T cells  Transplant immunology
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