IL15 and graft versus host disease: Although this mechanism could conceivably contribute to evolution of intestinal GVHD, ILC1 also require steady state transpresentation of IL-15 by FRCs for their survival (47); thus, the loss of tolerance in iFABPtOVA mice we observed following inducible FRC depletion in the absence of an inflammatory stimulus (Figure 6) is unlikely to be dependent on ILC1 activation.