Research ArticleFIBROSIS

Interleukin-36γ–producing macrophages drive IL-17–mediated fibrosis

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Science Immunology  11 Oct 2019:
Vol. 4, Issue 40, eaax4783
DOI: 10.1126/sciimmunol.aax4783

Sequencing in the matrix

Biological scaffolds that mimic tissue microenvironments can be used to model wound healing. Using two distinct biomaterial environments, one that promotes regeneration and another that promotes fibrosis in conjunction with single-cell RNA sequencing, Sommerfeld et al. have characterized macrophages involved in both fibrosis and regeneration. They have defined populations of macrophages that are involved in both processes, and they have identified a subset of CD9+ interleukin-36γ (IL-36γ)–producing macrophages that participate in IL-17–driven fibrosis. By evaluating wound healing in IL-17–deficient mice, they report IL-17 to be essential for the generation of CD9+ IL-36γ–producing macrophages during fibrosis. Further studies are needed to understand the functional relationship between IL-17– and IL-36γ–producing cells in fibrosis and in other settings.

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