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Adventitial fibroblast–ILC2 niche restrains liver fibrosis

Nature Reviews Immunology volume 23, page 477 (2023)Cite this article

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Fibrotic disease is a common outcome of chronic inflammation that affects almost all organ systems and is a contributing factor in 45% of all deaths in high-income countries. Fibrosis is regulated by diverse populations of fibroblasts — non-haematopoietic structural cells that define organ architecture and provide niches for tissue-resident cells. For example, a previous study showed that adventitial fibroblasts (AFs) produce IL-33 and TSLP to support tissue-resident populations of type 2 lymphocytes in the lung. However, the precise relationship between IL-33-producing AFs, tissue-resident lymphocytes and fibrotic disease is not well understood.

In this preprint (not peer-reviewed), Sbierski-Kind et al. use volumetric confocal microscopy and flow cytometry to show that IL-33high AFs represent a distinct fibroblast population in the steady-state liver, as well as in a carbon tetrachloride-induced model of liver fibrosis in mice. They show that expanding populations of IL-33high AFs, IL-5-producing group 2 innate lymphoid cells (ILC2s) and IL-17-producing γδ T cells colocalize during liver fibrosis in vivo. Moreover, they show that IL-33high AFs can maintain ILC2 and γδ T cell populations ex vivo. Taken together, these results show that IL-33high AFs provide a distinct stromal niche for IL-5+ ILC2s and IL-17+ γδ T cells in the liver.

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Original article

  • Sbierski-Kind, J. et al. Group 2 innate lymphoid cells constrain type 3/17 lymphocytes in shared stromal niches to restrict liver fibrosis. Preprint at bioRxiv https://doi.org/10.1101/2023.04.26.537913 (2023)

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  1. Preprint Club, University of Toronto, Toronto, Ontario, Canada

    Anthony Altieri & Matthew B. Buechler

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  1. Anthony Altieri
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  2. Matthew B. Buechler
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Correspondence to Anthony Altieri or Matthew B. Buechler.

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Altieri, A., Buechler, M.B. Adventitial fibroblast–ILC2 niche restrains liver fibrosis. Nat Rev Immunol 23, 477 (2023). https://doi.org/10.1038/s41577-023-00909-2

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  • DOI: https://doi.org/10.1038/s41577-023-00909-2

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