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. Author manuscript; available in PMC: 2012 Jul 21.
Published in final edited form as: Cell Host Microbe. 2011 Jul 21;10(1):44–53. doi: 10.1016/j.chom.2011.06.002

Figure 6. Proposed model to control IL-22 pathway against mucosal bacterial pathogen.

Figure 6

LT expression by RORγt+ ILCs is necessary for IL-22 production following invasion of mucosal bacterial pathogen. LT signaling by RORγt+ ILC promotes the development of lymphoid follicles in the gut. Lymphoid follicles provide necessary microenvironment for interaction between innate RORγt+ cells and DC. Interplay between RORγt+ ILCs and DCs promotes IL-23 production by DCs that, in turn, activates IL-22 synthesis by RORγt+ cells as a positive feedback loop. IL-22 stimulates IL-22R on epithelial cells which triggers production of antimicrobial proteins RegIIIγ and RegIIIβ to eliminate mucosal bacterial pathogen.