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. 2023 Jul 6;14:1219072. doi: 10.3389/fimmu.2023.1219072

Figure 1.

Figure 1

Pathogenic bacteria modulate ILC function through different mechanisms. Citrobacter rodentium produces the effect EspO which indirectly contributes to activation of ILC3s and their production of secreted IL-22 (7). As an intracellular pathogen Salmonella invades ILC3s which induces their pyroptosis and reduces their numbers in the GI tract (8). Toxin B (TcdB) produced by Clostridioides difficile directly activates ILC3s to produce IL-22 (9). Helicobacter pylori activates epithelial cells to produce IL-33 in a CagA-dependent manner. This IL-33 in turns activates ILC2s in the stomach to produce IL-5 (10, 11). Non-gastric Helicobacter species increase frequencies of cytokine producing ILC1s and ILC3s (12). Campylobacter infection induces conversion of ILC3s to ILC1s that can produce IFNγ (13). Bacillus anthracis secretes two toxins with opposing effects on ILC3s. Lethal toxin inhibits MAPK signaling which inhibits ILC3 activation (14). In contrast, edema toxin directly activates ILC3s to produce IL-22 (15). Direct interactions are shown with solid arrows, indirect interactions are shown with dashed arrows. Created with BioRender.com.