دورية أكاديمية
أعرض في EDS

Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis.

التفاصيل البيبلوغرافية
العنوان: Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis.
المؤلفون: Gieseck RL 3rd; Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA; Wellcome Trust-Medical Research Council Stem Cell Institute, Anne McLaren Laboratory, Department of Surgery, University of Cambridge, Cambridge CB2 0SZ, UK., Ramalingam TR; Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA., Hart KM; Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA., Vannella KM; Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA., Cantu DA; Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA., Lu WY; Medical Research Council Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK., Ferreira-González S; Medical Research Council Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK., Forbes SJ; Medical Research Council Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK., Vallier L; Wellcome Trust-Medical Research Council Stem Cell Institute, Anne McLaren Laboratory, Department of Surgery, University of Cambridge, Cambridge CB2 0SZ, UK; Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK., Wynn TA; Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA. Electronic address: twynn@niaid.nih.gov.
المصدر: Immunity [Immunity] 2016 Jul 19; Vol. 45 (1), pp. 145-58. Date of Electronic Publication: 2016 Jul 12.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Intramural
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 9432918 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4180 (Electronic) Linking ISSN: 10747613 NLM ISO Abbreviation: Immunity Subsets: MEDLINE
أسماء مطبوعة: Publication: Cambridge, MA : Cell Press
Original Publication: Cambridge, Mass. : Cell Press, c1994-
مواضيع طبية MeSH: Fatty Liver/*immunology , Fibroblasts/*immunology , Interleukin-13/*metabolism , Liver/*pathology , Liver Cirrhosis, Biliary/*immunology , Schistosoma mansoni/*immunology , Schistosomiasis mansoni/*immunology, Animals ; Bile Acids and Salts/biosynthesis ; Cell Proliferation ; Cells, Cultured ; Fibrosis ; Humans ; Interleukin-13/genetics ; Interleukin-13/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Signal Transduction ; Th2 Cells/immunology
مستخلص: 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. VIDEO ABSTRACT.
(Published by Elsevier Inc.)
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معلومات مُعتمدة: Z01 AI001019-01 United States ImNIH Intramural NIH HHS; Z01 AI000829-11 United States ImNIH Intramural NIH HHS; MC_PC_12009 United Kingdom MRC_ Medical Research Council; United Kingdom DH_ Department of Health; MR/K017047/1 United Kingdom MRC_ Medical Research Council; MR/K026666/1 United Kingdom MRC_ Medical Research Council
المشرفين على المادة: 0 (Bile Acids and Salts)
0 (Interleukin-13)
تواريخ الأحداث: Date Created: 20160717 Date Completed: 20170915 Latest Revision: 20220129
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4956513
DOI: 10.1016/j.immuni.2016.06.009
PMID: 27421703
قاعدة البيانات: MEDLINE
الوصف
تدمد:1097-4180
DOI:10.1016/j.immuni.2016.06.009