ArticleHepatology (Baltimore, Md.)2013
Clonality, activated antigen-specific CD8(+) T cells, and development of autoimmune cholangitis in dnTGFβRII mice.
Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Anti-kelch-like 12 and anti-hexokinase 1: novel autoantibodies in primary biliary cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2015Trial
- Effect of rapamycin nanoparticles in an animal model of primary biliary cholangitis.World journal of hepatology · 2025Article
- Targeting pathogenic CD8Nature communications · 2024Article
- Expression of E-cadherin by CD8Nature communications · 2024Article
- Animal models of primary biliary cholangitis: status and challenges.Cell & bioscience · 2023Review
- CD73, a significant protein in liver diseases.Frontiers in medicine · 2023Review
- Animal Models of Autoimmune Liver Diseases: a Comprehensive Review.Clinical reviews in allergy & immunology · 2020Review
- Liver-resident NK cells suppress autoimmune cholangitis and limit the proliferation of CD4Cellular & molecular immunology · 2020Article
- [Study the role of lysosome-associated membrane protein type 2A for immune-mediated liver injury of primary biliary cholangitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2018Article
- Anti-drug Antibodies Against a Novel Humanized Anti-CD20 Antibody Impair Its Therapeutic Effect on Primary Biliary Cholangitis in Human CD20- and FcγR-Expressing Mice.Frontiers in immunology · 2018Article
- Trichloroethylene Exposure Reduces Liver Injury in a Mouse Model of Primary Biliary Cholangitis.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Galectin-3 regulates inflammasome activation in cholestatic liver injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Endogenous interleukin-22 protects against inflammatory bowel disease but not autoimmune cholangitis in dominant negative form of transforming growth factor beta receptor type II mice.Clinical and experimental immunology · 2016Article
- A contemporary perspective on the molecular characteristics of mitochondrial autoantigens and diagnosis in primary biliary cholangitis.Expert review of molecular diagnostics · 2016Review
- Epigenetics and Primary Biliary Cirrhosis: a Comprehensive Review and Implications for Autoimmunity.Clinical reviews in allergy & immunology · 2016Review
- Adaptive immunity in the liver.Cellular & molecular immunology · 2016Review
- Xenobiotics and loss of tolerance in primary biliary cholangitis.World journal of gastroenterology · 2016Review
- Successful treatment of murine autoimmune cholangitis by parabiosis: Implications for hematopoietic therapy.Journal of autoimmunity · 2016Article
- Proposed therapies in primary biliary cholangitis.Expert review of gastroenterology & hepatology · 2016Review
- IL-35 and Autoimmunity: a Comprehensive Perspective.Clinical reviews in allergy & immunology · 2015Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
unlabelledThere are several murine models described with features similar to human primary biliary cirrhosis (PBC). Among these models, the one which has the closest serologic features to PBC is a mouse with a T-cell-restricted expression of the dominant negative transforming growth factor β receptor type II (dnTGFβRII). Our work has demonstrated that CD8(+) T cells from dnTGFβRII mice transfer autoimmune cholangitis to Rag1(-/-) recipients. However, it remained unclear whether the autoimmune cholangitis was secondary to an intrinsic function within CD8(+) T cells or due to the abnormal TGFβR environment within which CD8(+) T cells were generated. To address this mechanistic issue, we used our dnTGFβRII, OT-I/Rag1(-/-) , OT-II/Rag1(-/-) mice and in addition generated OT-I/dnTGFβRII/Rag1(-/-) , and OT-II/dnTGFβRII/Rag1(-/-) mice in which the entire T-cell repertoire was replaced with ovalbumin (OVA)-specific CD8(+) or CD4(+) T cells, respectively. Importantly, neither the parental OT-I/dnTGFβRII/Rag1(-/-) mice and/or OT-II/dnTGFβRII/Rag1(-/-) mice developed cholangitis. However, adoptive transfer demonstrated that only transfer of CD8(+) T cells from dnTGFβRII mice but not CD8(+) T cells from OT-I/Rag1(-/-) mice or from OT-I/dnTGFβRII/Rag1(-/-) mice transferred disease. These data were not secondary to an absence of CD4(+) T cell help since a combination of CD8(+) T cells from OT-I/dnTGFβRII/Rag1(-/-) and CD4(+) T cells from OT II/dnTGFβRII/Rag1(-/-) or CD8(+) T cells from OT-I/dnTGFβRII/Rag1(-/-) with CD4(+) T cells from OT-II/Rag1(-/-) mice failed to transfer disease.
conclusionDefective TGFβRII signaling, in addition to clonal CD8(+) T cells that target biliary cells, are required for induction of autoimmune cholangitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.