Autoimmune Hepatitis
Autoimmune Hepatitis - Related Videos
09:03
The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
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Cited by 31 •
2012
Infection of mice with an Adenovirus expressing the major human autoantigen cytochrome P450 2D6 (hCYP2D6) recognized by sera of patients suffering from type 2 autoimmune hepatitis results in a persistent form of autoimmune-mediated liver disease characterized by extensive hepatitis, fibrosis and generation of a CYP2D6-specific immune response.
11:36
Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms
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Cited by 6 •
2020
We describe an in vivo immunization, translational hepatitis model in BALB/c mice that can be utilized to study the pathogenesis of drug-induced autoimmune hepatitis including sex differences seen in this disease. We will describe how this model demonstrates reproducible analyses using in vivo and in vitro experimental techniques.
09:35
Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
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Cited by 2 •
2017
Here we describe a newly developed hepatitis B virus (HBV) reporter system to monitor the early stages of the HBV life cycle. This simplified in vitro system will aid in the screening of anti-HBV agents using a high-throughput strategy.
10:38
Induction of Experimental Autoimmune Hypophysitis in SJL Mice
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Cited by 4 •
2010
This video shows how to induce autoimmune hypophysitis in SJL mice and how to assess its severity by histopathology.
10:40
Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
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Cited by 10 •
2012
An optical system was developed to visualize hepatic microcirculation with FITC-labeled erythrocytes and to measure the partial pressure of oxygen in the microvessels with laser-assisted phosphorimetry. This method can be used to investigate physiological and pathological mechanisms by analyzing microvascular structure, diameter, blood flow velocity, and oxygen tension.
FAQs
Loss of immune tolerance allows the immune system to recognize liver components as targets rather than preserving the normal distinction between self and nonself. Autoreactive lymphocytes can then sustain inflammation and hepatocellular injury. Over time, continuing injury may promote progressive fibrosis, which can compromise liver structure and contribute to cirrhosis.
Autoreactive lymphocytes contribute directly to immune-mediated inflammation against liver cells, while autoantibodies provide evidence of the abnormal immune response. Together, these features reflect a breakdown in organ-specific immune regulation rather than an isolated laboratory abnormality. Their presence helps place the liver injury within an autoimmune biological context.
Elevated aminotransferases indicate hepatocellular injury, whereas increased immunoglobulin G reflects an associated alteration in the immune response. Neither finding alone establishes the disease, but their combination can support clinical evaluation when interpreted with other evidence. These measurements also help characterize the inflammatory process affecting liver cells.
Differentiation requires considering the immune findings together with laboratory results and, when needed, liver biopsy. Viral, metabolic, and drug-induced injuries can produce overlapping evidence of liver damage, so the diagnostic process must evaluate whether the overall pattern supports immune-mediated disease. This distinction matters because the underlying cause guides subsequent management.
Liver biopsy can help confirm the diagnosis after clinical and laboratory findings raise concern for autoimmune disease. It provides additional information about the liver tissue and the extent of injury, including whether progressive fibrosis may be present. In practice, biopsy supports diagnostic clarification when other causes of liver injury remain possible.
Immunosuppressive treatment aims to reduce the immune-driven inflammation responsible for ongoing liver injury. By limiting this process, therapy can help preserve liver function and reduce the risk of long-term complications associated with progressive damage. Severe disease may exceed the capacity of medical treatment and require consideration of transplantation.
The disease provides a model for examining how immune regulation fails in an organ-specific condition. It connects cellular immune responses, autoantibody production, tissue injury, fibrosis, and clinical laboratory findings within one biological system. Studying these relationships also supports the differentiation of autoimmune injury from viral, metabolic, and drug-related causes of liver disease.