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. 2021 Aug 24;28(3):434–446. doi: 10.1093/ibd/izab193

Figure 7.

Figure 7.

Precision medicine proposed mechanism of action for PF-06480605. We hypothesize the following mechanisms of action for PF-06480605: (1) inflammatory MΦ are increased in IBD and produce IL-23, IL-1B, and TL1A. Interleukin-1B can feed back in an autocrine fashion to promote cytokine production. (2) TL1A stimulates pathogenic Th17 and mediates ILC3 and regulates Th1 through either OX40/OX40L or via the transitioning of ILC3 to ILC1 and the production of interferon gamma. (3) Additionally, TL1A and IL-33 regulate ILC2, which contributes to the Th2-driven IL-13 response, matrix metalloproteinase activation, tissue remodeling, and fibrosis. (4) TL1A stimulates fibroblast proliferation and contributes to fibrosis. (5) By blocking TL1A, we inhibit inflammation, inflammatory macrophage requirement, and fibrosis. Abbreviations: IBD, inflammatory bowel disease; IL, interleukin; ILC, innate lymphoid cell; Inf, inflamed; MΦ, macrophages; TL1A, tumor necrosis factor-like ligand 1A.