ReviewAutoimmunity reviews
B and T cells: (Still) the dominant orchestrators in autoimmune hepatitis.
Review in Autoimmunity reviews. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Review article: Immunosuppression in Decompensated Autoimmune Hepatitis Cirrhosis - To Suppress or Not to Suppress?Alimentary pharmacology & therapeutics · 2026Review
- Immunomodulatory effects of tacrolimus-loaded lipid-core nanocapsules in autoimmune hepatitis.Journal of autoimmunity · 2026Article
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- Regulatory T-cells in autoimmune hepatitis: An historical perspective with hints to the future.JHEP reports : innovation in hepatology · 2026Article
- Network pharmacological and experimental validation of the mechanism of Chaihu Guizhi Ganjiang decoction regulating T helper cell 17/regulatory T cell balance to improve autoimmune hepatitis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Ubiquitin-Conjugating Enzyme E2O Primes Hepatocytes to Restore Immune Tolerance in Autoimmune Hepatitis via Inhibiting Y-Box Binding Protein 1/Interleukin-6 Axis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Revealing the pathogenesis of autoimmune hepatitis and research progress in drug discovery from hepatic immune cells and intercellular communication signaling mechanisms.Frontiers in immunology · 2026Review
- Tryptophan catabolites from microbiota ameliorate immune-mediated hepatitis through activating aryl hydrocarbon receptor of T cells.Gut microbes · 2025Article
- Mendelian randomization of autoimmune hepatitis and cardiovascular diseases.American heart journal plus : cardiology research and practice · 2025Article
- Clinical and laboratory characteristics of Sjögren's syndrome-associated autoimmune liver disease: a real-world, 10-year retrospective study.Clinical rheumatology · 2025Article
- Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.Frontiers in cell and developmental biology · 2025Review
- Metabolism of hepatic stellate cells in chronic liver diseases: emerging molecular and therapeutic interventions.Theranostics · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Autoimmune hepatitis (AIH) is a severe hepatopathy characterized by hypergammaglobulinemia, presence of serum autoantibodies and histological appearance of interface hepatitis. Liver damage in AIH is initiated by the presentation of a liver autoantigen to uncommitted Th0 lymphocytes, followed by a cascade of effector immune responses culminating with the production of inflammatory cytokines, activation of cytotoxic cells and subsequent hepatocyte injury. B cells actively participate in AIH liver damage by presenting autoantigens to uncommitted T lymphocytes. B cells also undergo maturation into plasma cells that are responsible for production of immunoglobulin G and autoantibodies, which mediate antibody dependent cell cytotoxicity. Perpetuation of effector immunity with consequent progression of liver damage is permitted by impairment in regulatory T cells (Tregs), a lymphocyte subset central to the maintenance of immune homeostasis. Treg impairment in AIH is multifactorial, deriving from numerical decrease, reduced suppressive function, poor response to IL-2 and less stable phenotype. In this review, we discuss the role of B and T lymphocytes in the pathogenesis of AIH. Immunotherapeutic strategies that could limit inflammation and halt disease progression while reconstituting tolerance to liver autoantigens are also reviewed and discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.