Autoimmune hepatitis is an autoimmune disease that was proposed by the Autoimmune Hepatitis Group at the International Conference on Digestive Systems in the United Kingdom in 1992 as an alternative to autoimmune active hepatitis. It is a disease of unknown etiology. It is generally believed that under the action of environmental pathogenic factors such as viral infections, drugs or chemicals, the antigenic components of the hepatocytes of people genetically susceptible to autoimmune hepatitis are altered, or certain viral proteins have homology with certain protein components of the hepatocytes, thus inducing an autoimmune response in the body and leading to liver damage. The main features are: 1. hyperimmunoglobulinemia; 2. the appearance of tissue autoantibodies; 3. the effectiveness of immunosuppressive therapy. Liver function tests in patients with autoimmune hepatitis show: serum bilirubin is often mildly or moderately increased, serum transaminases, γ-glutamyl transpeptidase and adenosine deaminase are often elevated, γ-globulin is significantly increased, IgG is elevated, but albumin is mostly normal. A variety of autoantibodies can be measured in AIH patients, the most classic being anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (SMA) and anti-liver-kidney microsomal antibodies (anti-LKM). Other related autoantibodies include anti-hepatic-pancreatic antibodies, anti-soluble liver antigen antibodies, anti-hepatic cytosolic antigen type I, and anti-neutrophil cytoplasmic antibodies. The pathological manifestation of AIH is not very specific, but it is crucial for the diagnosis and severity of AIH. Therefore, the pathological findings of liver biopsy remain one of the important criteria for the diagnosis of AIH. the main pathological features of AIH are infiltration of single nucleated cells in the portal area, mainly invading the border plate and confluent area of the liver lobules, and invasion of the lobules, resulting in periportal or periportal debris-like necrosis, and sometimes bridge-like necrosis in the portal-portal or portal-lobular central area. These pathological changes, although characteristic, can only be suggestive and not specific to AIH, and are also seen in chronic viral hepatitis, drug-induced hepatitis, and many other liver diseases. AIH can be divided into 3 types according to the type of autoantibodies in the serum. Type I AIH: It accounts for about 80-85% of all AIH patients. Seventy percent of them are female patients, and their age is usually less than 40 years. The main diagnostic features are ANA and SMA positivity, of which anti-actin antibodies, especially anti-polymeric F-actin, are the most specific for diagnosis. In 17% of these patients, there is a combination of other autoimmune diseases, and it has been suggested that this type of disease may be a combination of connective tissue disease and liver damage. 42% of patients may present with primary sclerosing cholangitis. This type has a slow onset and responds well to glucocorticoid therapy. Type II AIH: It accounts for about 5% of the total number of AIH patients. It is mostly seen in children aged 2-14 years and is more prevalent in Western Europe (France, Germany). The main features are anti-LKM1 and anti-LC-1 positivity. Type II has a more severe clinical presentation than type I, progresses more rapidly, has more fulminant hepatitis, is more likely to progress to cirrhosis, and is less responsive to glucocorticoid therapy than type I. Many reports suggest that HCV infection is related to type II AIH. 3. Type III AIH: 90% are young women. The main features are anti-SLA and anti-LP positive, mostly without anti-LKM1, but 74% may have SMA or ANA positive. The effect of this type on drug therapy is similar to that of type I.