However, Dwyer et al. [272] reported that IL-33 promoted IL-12-independent T bet expression and Th1 cell polarization in response to alloantigens by augmenting the TCR-associated signaling pathways and inhibiting the expression of regulatory molecules, such as IL-10 and Foxp3, in a GVHD mouse model. Here, IL33 is linked to graft versus host disease.