We study how the suppressive function of Treg is controlled

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Dr. Benoit Salomon and his group have been working for more than 20 years on the biology and function of Foxp3-expressing regulatory T cells (Treg) in the mouse. They have shown that these cells play a major role in the control of type 1 diabetes, graft-versus-host disease or atherosclerosis and have contributed to a better characterisation of the effect of IL-2 and TNF on Treg biology and the therapeutic implications of these effects. 
The current projects of the group are a continuation of this work to better understand the biology of Treg homeostasis and the mechanisms involved in their ability to control autoimmune diseases and anti-tumour responses. Our projects are organized around 4 axes. 1- Study of the biology and function of "ex-Treg", a population of conventional T cells that were Treg at some point in their life and have lost this status. 2- Study of the metabolic adaptation of Treg in non-lymphoid tissues. 3- Study of the mechanisms of Treg-mediated suppression in autoimmune diseases and cancers involving molecules of the TNF family. 4- Study of new therapeutic approaches for these diseases involving Treg. 
Most of these projects are carried out using genetically modified mice in which the expression of a gene of interest is specifically suppressed in Tregs. We have generated conditional KO mice for TNF family receptors (TNFR2, 4-1BB), co-stimulatory molecules (ICOS) or metabolic molecules (AMPK, LKB1). As a reference autoimmune disease model, we use the experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. These projects require the use of multiparametric flow cytometry and transcriptomics technology.