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Sbierski-Kind, J. ; Cautivo, K.M.* ; Nilsson, J.* ; Wagner, J.C.* ; Dahlgren, M.W.* ; Crystal, N.E.* ; McClave, M.* ; Mroz, N.M.* ; Ganslmeier, M. ; Lizama, C.O.* ; Gan, A.L.* ; Matatia, P.R.* ; Taruselli, M.T.* ; Chang, A.A.* ; Caryotakis, S.* ; O'Leary, C.E.* ; Kotas, M.* ; Lee, J.H.* ; Gu, T.* ; Seo, H.* ; Kim, H.J.* ; Mattis, A.N.* ; Peng, T.* ; Locksley, R.M.* ; Molofsky, A.B.*

Type 2 lymphocytes restrict type 3 lymphocytes during liver fibrosis and colocalize in fibroblast niches.

Sci. Adv. 12:eaea6805 (2026)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Fibroblasts are dynamic structural cells that direct both beneficial tissue repair and pathological organ fibrosis through interactions with tissue-resident type 2 lymphocytes (T2Ls) and type 3/17 lymphocytes (T3Ls). The cytokines interleukin-13 (IL-13) and IL-17A, produced by T2Ls and T3Ls, respectively, are linked to both tissue inflammation and fibrosis, but how their spatial positioning influences beneficial or pathological organ remodeling remains unclear. Using mouse models of liver injury and fibrosis, three-dimensional microscopy, and spatial transcriptomics, we found an accumulation of periportal and fibrotic tract T2Ls, predominantly group 2 innate lymphoid cells (ILC2s), positioned near T3Ls and niche adventitial fibroblasts and adjacent to discrete profibrotic myofibroblasts. Unexpectedly, T2L ablation worsened both carbon tetrachloride- and bile duct ligation-induced liver fibrosis, accompanied by increased IL-17A+ T3Ls, predominantly γδ T cells. In contrast, concurrent T2L and T3L ablation reduced liver fibrosis. Our work suggests a spatially associated cross-talk between liver lymphocytes and fibroblast niches that tunes liver repair but can go awry in pathological liver fibrosis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Innate Lymphoid-cells; Hepatic Stellate Cells; Tissue-repair; Proinflammatory Il-17(+); Protective Role; Kupffer Cells; Receptor; Macrophages; Expression; Bleomycin
ISSN (print) / ISBN 2375-2548
e-ISSN 2375-2548
Zeitschrift Science Advances
Quellenangaben Band: 12, Heft: 11, Seiten: , Artikelnummer: eaea6805 Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Verlagsort Washington, DC [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)
Förderungen Swedish Research Council
Nina Ireland Program for Lung Health
Larry L. Hillblom Foundation Grant
NIDDK
NLHBI
Swedish Research Council (Vetenskapsradet)
German Society of Internal Medicine
LMU Munich
FoeFoLe
Vinnova
UCSF PBBR grant
UCSF RAP grant
CIRM grant
UCSF Liver Center grant
Creative-Pioneering Researchers Program through Seoul National University
Sandler Asthma Basic Research Center (SABRE)
NIH
German Research Foundation