期刊
IMMUNITY
卷 45, 期 1, 页码 145-158出版社
CELL PRESS
DOI: 10.1016/j.immuni.2016.06.009
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资金
- Intramural Research Program of the NIH, National Institute of Allergy and Infectious Disease
- ERC
- Cambridge Hospitals National Institute for Health Research Biomedical Research Center
- UKRMP Hub
- Medical Research Council
- MRC [MR/K026666/1, MR/K017047/1] Funding Source: UKRI
- Medical Research Council [MC_PC_12009, MR/K017047/1, MR/K026666/1] Funding Source: researchfish
Fibroproliferative diseases are driven by dysregulated tissue repair responses and are a major cause of morbidity and mortality because they affect nearly every organ system. Type 2 cytokine responses are critically involved in tissue repair; however, the mechanisms that regulate beneficial regeneration versus pathological fibrosis are not well understood. Here, we have shown that the type 2 effector cytokine interleukin-13 simultaneously, yet independently, directed hepatic fibrosis and the compensatory proliferation of hepatocytes and biliary cells in progressive models of liver disease induced by interleukin-13 overexpression or after infection with Schistosoma mansoni. Using transgenic mice with interleukin-13 signaling genetically disrupted in hepatocytes, cholangiocytes, or resident tissue fibroblasts, we have revealed direct and distinct roles for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction. Together, these studies show that these mechanisms are simultaneously controlled but distinctly regulated by interleukin-13 signaling. Thus, it may be possible to promote interleukin-13-dependent hepatobiliary expansion without generating pathological fibrosis.
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