Next, in agreement with the findings that CD4+ T cells are required for the development of CeD, the prevention of villous atrophy in DQ8-Dd-villin-IL-15tg mice treated with an anti-CD4 depleting antibody, anti-IFNγ depleting antibody or TG2 inhibitors concomitantly to gluten administration also underlined the existence of a cross-talk between TH1 immunity in the lamina propria and the activation of IE-CTLs (23). Here, TGM2 is linked to cranioectodermal dysplasia.