However, the inability of both Rorc-MyDON and LysM-MyDON mice to activate substantial host response mechanisms upon infection clearly suggests that the pronounced establishment of the immune response that we observed in CD11c-MyDON mice was not a consequence of functional MyD88 expression in T cells, ILC3 or MO, but indeed due to functional MyD88 signaling in DC. Here, MYD88 is linked to infection.