There are four types of metabolic reactions according to the different mechanisms of immune damage: 1. Type I (IgE-mediated): the combination of IgE antibodies adsorbed on the surface of mast cells/basophils and the corresponding antigens causes the cells to release histamine, leukotrienes and other bioactive mediators causing smooth muscle contraction, increased glandular secretion, dilation of small vessels and capillaries, increased permeability, eosinophilia, infiltration, and the reaction The process generally does not destroy tissue cells. The main sites of lesions are the skin, respiratory tract, gastrointestinal tract and cardiovascular system. Therefore, the clinical manifestations are often urticaria (skin), asthma, allergic rhinitis (respiratory tract), nausea and vomiting, abdominal pain and diarrhea (digestive tract) and anaphylaxis. 2. Type II (antibody-mediated cytotoxic type): The target cell surface antigen or semi-antigen binds to the target cell to form a complete antigen to stimulate the body to produce antibodies (IgG/IgM/IgA), and then encounters the same target cell antigen or semi-antigen adsorbed on the cell membrane to activate complement to lyse the cell. The most commonly involved are red blood cells such as autoimmune hemolytic anemia, neonatal hemolytic disease; followed by granulocytes/platelets, such as aminopyrin-induced granulocytopenia, and thrombocytopenic purpura caused by siderophores. 3, Type III (immune complex type): Non-cellular antigens form soluble immune complexes with antibodies (IgG/IgM) in the blood circulation, which are deposited in the vessel wall or basement membrane causing complement activation, attracting neutrophil aggregation and releasing lysosomes, resulting in vascular inflammation and tissue damage at the site of complex deposition. The lesions are dominated by edema, cellular infiltration, and hemorrhagic necrosis. The pathogenesis of acute glomerulonephritis, systemic lupus erythematosus, and rheumatoid arthritis is of this type. Type IV (cellular reactive or delayed type): This type is different from the first three types and has nothing to do with antibodies. It is the release of various lymphokines (transfer factors, macrophage movement inhibitory factors, etc.) by sensitized lymphocytes (TD) in combination with the corresponding antigen, and cytotoxic T cells (TC) can also directly kill the target cells, resulting in a metaplastic inflammation characterized by infiltration of single nucleated cells and cellular degeneration and necrosis. This type of reaction is delayed and usually occurs 12-24 hours after re-exposure to the antigen, with a peak reaction at 48-72 hours, as in contact dermatitis.