CXCL1 and enteritis: These studies indicated that induction of TLR2 activity with a prototypical TLR2 ligand (Pam2CSK4) evoked CXCL1 production in Atg16l1-deficient IECs and enteritis in our model, suggesting that ATG16L1 controlled TLR2 activity upstream of this receptor while being dispensable for execution of TLR2 (downstream) signaling.