Fig. 3.

Overview of NOD1-, NOD2-, and NLRP3 inflammasome-mediated signalling. Upon activation in response to certain phosphorylated fragments of peptidoglycan, NOD1 and NOD2 trigger pro-inflammatory gene expression programs via NF-κB and mitogen-activated protein kinase pathways (left) [38]. The NLRP3 inflammasome (right) requires priming and then activation in response to signals 1 and 2, respectively [100]. Following inflammasome assembly, autoactivated caspase-1 cleaves (i) the precursors of IL-1β and IL-18, generating their mature forms, and (ii) Gasdermin D, liberating the N-terminal fragment that creates membrane pores and induces pyroptosis, an inflammatory mode of cell death [100]. Both NOD2 and NLRP3 activation have important consequences for adaptive immune responses (yellow boxes), as detailed in the main text. Abbreviations: AP-1, activator protein 1; ERK, extracellular signal-regulated kinase; GSDMD, Gasdermin D; IκB, inhibitor of NF-κB; JNK, c-Jun N-terminal kinase; NF-κB, nuclear factor-κB; N-GSDMD, N-terminal fragment of Gasdermin D; NLRP3, NOD-, LRR- and pyrin domain-containing protein 3; and NOD2, nucleotide-binding oligomerization domain-containing protein 2. Created with BioRender.com.