Skip to main content
Figure 1 | Cell Communication and Signaling

Figure 1

From: H. pylori exploits and manipulates innate and adaptive immune cell signaling pathways to establish persistent infection

Figure 1

Host innate immune receptors and signaling networks known or believed to participate in H. pylori recognition. Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-like receptors (RLRs), and C-type lectin receptors (CLRs) are expressed on the cell surface, in the endosomes, or in the cytosol of various types of immune cells. Their activation by specific pathogen-associated molecular patterns/ligands induces the expression of cytokine genes or results in the activation of caspase-1 and processing of IL-1β and IL-18. TLR2 and TLR9 recognize H. pylori LPS, lipoproteins and DNA, respectively [8–11]; in contrast, H. pylori LPS and flagellins are poor ligands of TLR4 and TLR5, respectively (indicated by dotted lines) [5, 7]. The RIG-I-dependent recognition of H. pylori 5'-triphosphorylated RNA in dendritic cells has been reported to induce expression of type I interferons [10]; fucosylated H. pylori ligands for the CLR DC-SIGN have been described, but appear to repress rather than activate signaling downstream of this surface-exposed CLR [12]. NOD1 recognizes H. pylori peptidoglycan and activates the transcription factors NF-κB and AP1 [16, 17], and also triggers the production of type I interferons [21]. Comparatively little is known regarding additional possible NLR ligands (indicated by question marks). Conceivable, but unconfirmed H. pylori NLR ligands include flagellins (for NAIP5 and IPAF) and toxins (NALP3), which would activate the inflammasome and lead to the secretion of mature IL-1β and IL-18. Adapted from [1].

Back to article page