A better understanding of immune mechanisms involved in allograft rejection or tolerance has to be considered as a major research goal. This knowledge could lead to the design of new therapeutical approach that could be used in the future to replace immunosuppressive treatment.  Thomas Condamine and his research team have studied the potential role of two molecules upregulated in a model of cardiac allograft tolerance in the rat: The Follistatin-Like 1 (FSTL1) and TORID. They have shown that FSTL1 is produced by graft infiltrating CD8^+ T cells in this model and that FSTL1 could induce a prolonged allograft survival in association with inhibition of the proinflammatory cytokines, IL6, IL17 and IFNγ. In the study of the molecule TORID, Thomas Condamine and his colleagues have been able to show a role of this molecule in the maturation of dendritic cells (DC) and a role on the regulation, of previously described, immunomodulatory enzymes in myeloid derived suppressor cells (MDSC). In addition, in a model of skin graft tolerance induction involving MDSC, they have shown that they can not induce a tolerance in TORID deficient mice.