Figure 3. ILC1s express T-bet and IFN-γ and contribute to type 1 inflammation. T-bet–expressing ILC1s develop from a progenitor that expresses PLZF and Id2 and responds to IL-15. RORγt-expressing cells can also lose expression of RORγt and gain expression of T-bet in response to IL-12 signaling (ex-ILC3s). T-bet–expressing ILCs with a history of RORγt expression or T-bet+ ILC1s respond to IL-12 and IL-15 to produce IFN-γ that is protective during infection with pathogens such as C. difficile, T. gondii, and hepatitis B (not depicted: T-bet–expressing ILCs that currently or previously expressed RORγt are specifically important during infection with S. enterica as well, though these ILCs are more ILC3 like) and may contribute to inflammation and pathology in the intestine in the context of IBD.
Figure 3.

ILC1s express T-bet and IFN-γ and contribute to type 1 inflammation. T-bet–expressing ILC1s develop from a progenitor that expresses PLZF and Id2 and responds to IL-15. RORγt-expressing cells can also lose expression of RORγt and gain expression of T-bet in response to IL-12 signaling (ex-ILC3s). T-bet–expressing ILCs with a history of RORγt expression or T-bet+ ILC1s respond to IL-12 and IL-15 to produce IFN-γ that is protective during infection with pathogens such as C. difficile, T. gondii, and hepatitis B (not depicted: T-bet–expressing ILCs that currently or previously expressed RORγt are specifically important during infection with S. enterica as well, though these ILCs are more ILC3 like) and may contribute to inflammation and pathology in the intestine in the context of IBD.

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