Anti-cardiac antibody

As early as 1937, Brokman et al., When studying rheumatic fever, used saline-extracted heart tissue extract as an antigen and established a complement binding test. Anti-cardiac antibodies were detected in 82% of rheumatic fever patients. For more than 60 years, research in this area has been uninterrupted. In addition to the classic indirect immunofluorescence test (taking human and rat heart tissues as antigen pieces), it has also used collodion particle agglutination test, anti-ball Protein depletion tests, tannin-treated or aldehyde-formed erythrocyte agglutination tests, and ELISA and immunoblotting techniques used in recent years, etc., but due to the complex antigenic components of myocardial tissue, corresponding autoantibodies are also diverse. Previous research has roughly used four methods: ① antiserum obtained after immunizing animals with human heart or skeletal muscle tissue extract; ② immunizing rabbit antisera with group A streptococci; ③ patients with rheumatic heart disease and streptococcal infection Postoperative patients, patients after cardiac surgery, patients with myocardial infarction syndrome; ④ The serum of patients with connective tissue disease (such as polymyositis) and myasthenia gravis was studied. turn out. Antibodies obtained by immunizing rabbits with myocardial infusion or group A streptococcal cell wall can cause three types of immunofluorescence: ① peripheral sarcoplasmic / sarcolemmal staining; ② myocardial or skeletal muscle myofibrils Intermyofibrillar staining; ③ Smooth muscle staining is rare. Connective tissue disease (rheumatoid arthritis, systemic lupus erythematosus), liver disease (primary biliary cirrhosis) patients' serum can produce myocardial and skeletal muscle diffuse myofibrillar immunofluorescence, serum from patients with myasthenia gravis Can make skeletal muscle horizontal stripes (A band) stained with fluorescence. Anti-mitochondrial antibodies in the serum of patients with primary biliary cirrhosis can also cause strong myofibrillar fluorescence in the heart muscle. The above studies indicate that the anti-cardiac antibodies previously measured lack tissue specificity and disease specificity. In the early 1990s, some people extracted myocardial cell membrane antigens from rat myocardium, and confirmed by immunoblot technology that anti-cardiac antibodies in the serum of patients with viral myocarditis and dilated cardiomyopathy can interact with calcium channel peptides and β1 in myocardial cell membrane antigens. -Adrenergic receptor response. In 1989, Schulze et al. Reported that patients with dilated cardiomyopathy had autoantibodies against the myocardial mitochondrial ADP / ATP vector (adenine nucleotide translocation enzyme, ANT). ANT is a protein in the inner membrane of the mitochondria. Its function is to transport ATP to the cytoplasm for energy, and at the same time transfer ADP in the cytoplasm to the mitochondria for phosphorylation. Anti-ANT antibodies can affect ANT function and make the energy supply and demand of cardiomyocytes out of balance. Recently, some people in China have used immunoblotting to find that children with viral myocarditis have anti-ANT antibodies accounting for about 1/4.

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