ArticleJournal of immunology (Baltimore, Md. : 1950)2011
CD8 T cells mediate direct biliary ductule damage in nonobese diabetic autoimmune biliary disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Genetic Polymorphisms of Cytotoxic T-Lymphocyte Antigen 4 in Primary Biliary Cholangitis: A Meta-Analysis.Journal of immunology research · 2017Pooled it
- Effect of rapamycin nanoparticles in an animal model of primary biliary cholangitis.World journal of hepatology · 2025Article
- Targeting pathogenic CD8Nature communications · 2024Article
- The effects of low-dose IL-2 on Th17/Treg cell imbalance in primary biliary cholangitis mouse models.BMC gastroenterology · 2024Article
- Article
- Treatment with a JAK1/2 inhibitor ameliorates murine autoimmune cholangitis induced by IFN overexpression.Cellular & molecular immunology · 2022Article
- The NOD Mouse Beyond Autoimmune Diabetes.Frontiers in immunology · 2022Review
- Animal Models of Autoimmune Liver Diseases: a Comprehensive Review.Clinical reviews in allergy & immunology · 2020Review
- Primary biliary cholangitis: pathogenesis and therapeutic opportunities.Nature reviews. Gastroenterology & hepatology · 2020Review
- Suppression of a broad spectrum of liver autoimmune pathologies by single peptide-MHC-based nanomedicines.Nature communications · 2019Article
- Endogenous IL-10 maintains immune tolerance but IL-10 gene transfer exacerbates autoimmune cholangitis.Journal of autoimmunity · 2018Article
- Co-occurrence of opisthorchiasis and diabetes exacerbates morbidity of the hepatobiliary tract disease.PLoS neglected tropical diseases · 2018Article
- Improvement of primary biliary cholangitis (PBC) under treatment with sulfasalazine and abatacept.BMJ case reports · 2018Article
- The interplay of type I and type II interferons in murine autoimmune cholangitis as a basis for sex-biased autoimmunity.Hepatology (Baltimore, Md.) · 2018Article
- A NovelJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- CD8 T cells contribute to lacrimal gland pathology in the nonobese diabetic mouse model of Sjögren syndrome.Immunology and cell biology · 2017Article
- The role of natural killer T cells in a mouse model with spontaneous bile duct inflammation.Physiological reports · 2017Article
- Dual Roles of IFN-γ and IL-4 in the Natural History of Murine Autoimmune Cholangitis: IL-30 and Implications for Precision Medicine.Scientific reports · 2016Article
- A New Mouse Model That Spontaneously Develops Chronic Liver Inflammation and Fibrosis.PloS one · 2016Article
- The Distribution and the Fibrotic Role of Elevated Inflammatory Th17 Cells in Patients With Primary Biliary Cirrhosis.Medicine · 2015Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
We previously described the NOD.c3c4 mouse, which is protected from type 1 diabetes (T1D) because of protective alleles at multiple insulin-dependent diabetes (Idd) genes, but develops autoimmune biliary disease (ABD) resembling primary biliary cirrhosis (PBC). In this paper, we characterize the NOD.ABD strain, which is genetically related to the NOD.c3c4 strain but develops both ABD and T1D. Histologically, NOD.ABD biliary disease is indistinguishable from that in NOD.c3c4 mice. The frequency of effector memory (CD44(+)CD62L(-)) and central memory (CD44(+)CD62L(+)) CD8 T cells is significantly increased in the intrahepatic lymphocyte fraction of NOD.ABD mice, and NOD.ABD CD8 T cells produce more IFN-γ and TNF-α, compared with controls. NOD.ABD splenocytes can transfer ABD and T1D to NOD.c3c4 scid mice, but only T1D to NOD scid mice, suggesting that the genetic origin of the target organ and/or its innate immune cells is critical to disease pathogenesis. The disease transfer model, importantly, shows that biliary duct damage (characteristic of PBC) and inflammation precede biliary epithelial cell proliferation. Unlike T1D where both CD4 and CD8 T cells are required for disease transfer, purified NOD.ABD CD8 T cells can transfer liver inflammation into NOD.c3c4 scid recipients, and disease transfer is ameliorated by cotransferring T regulatory cells. Unlike NOD.c3c4 mice, NOD.ABD mice do not develop anti-nuclear or anti-Smith autoantibodies; however, NOD.ABD mice do develop the antipyruvate dehydrogenase Abs typical of human PBC. The NOD.ABD strain is a model of immune dysregulation affecting two organ systems, most likely by mechanisms that do not completely coincide.
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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.