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© Research
Publication : Nature medicine

XCR1+ type 1 conventional dendritic cells drive liver pathology in non-alcoholic steatohepatitis.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature medicine - 20 May 2021

Deczkowska A, David E, Ramadori P, Pfister D, Safran M, At The B, Giladi A, Jaitin DA, Barboy O, Cohen M, Yofe I, Gur C, Shlomi-Loubaton S, Henri S, Suhail Y, Qiu M, Kam S, Hermon H, Lahat E, Ben Yakov G, Cohen-Ezra O, Davidov Y, Likhter M, Goitein D, Roth S, Weber A, Malissen B, Weiner A, Ben-Ari Z, Heikenwälder M, Elinav E, Amit I,

Link to Pubmed [PMID] – 34017133

Link to DOI – 10.1038/s41591-021-01344-3

Nat Med 2021 May; ():

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are prevalent liver conditions that underlie the development of life-threatening cirrhosis, liver failure and liver cancer. Chronic necro-inflammation is a critical factor in development of NASH, yet the cellular and molecular mechanisms of immune dysregulation in this disease are poorly understood. Here, using single-cell transcriptomic analysis, we comprehensively profiled the immune composition of the mouse liver during NASH. We identified a significant pathology-associated increase in hepatic conventional dendritic cells (cDCs) and further defined their source as NASH-induced boost in cycling of cDC progenitors in the bone marrow. Analysis of blood and liver from patients on the NAFLD/NASH spectrum showed that type 1 cDCs (cDC1) were more abundant and activated in disease. Sequencing of physically interacting cDC-T cell pairs from liver-draining lymph nodes revealed that cDCs in NASH promote inflammatory T cell reprogramming, previously associated with NASH worsening. Finally, depletion of cDC1 in XCR1DTA mice or using anti-XCL1-blocking antibody attenuated liver pathology in NASH mouse models. Overall, our study provides a comprehensive characterization of cDC biology in NASH and identifies XCR1+ cDC1 as an important driver of liver pathology.

https://pubmed.ncbi.nlm.nih.gov/34017133