Figure 2.

Toll-like receptors (TLRs) and Nod-like receptors (NLRs) regulate autophagy and the innate immune responses. Pathogens are identified by TLRs and NLRs. TLRs activate NF-κB through MyD88-dependent pathways, leading to the production of pro-inflammatory cytokines and the formation of autophagosomes that sequester intracellular p athogens. NLRs recognize cytosolic bacteria. The NLRs NOD1 and NOD2 detect γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP) and muramyl dipeptide (MDP), respectively, and induce autophagosome formation. In this step, ATG16L1 facilitates bacterial trafficking. The pathogens are ultimately removed through autophagy.