Kawasaki disease, also known as mucocutaneous lymph node syndrome, has an unclear pathogenesis. It is speculated that certain components of infectious sources, such as superantigens, can activate CD30 T cells and CD40 ligand expression directly by binding with T cell antigen receptor fragments without going through mononuclear macrophages. Under the induction of carrier cells, there is polyclonal activation and reduced apoptosis of B08 cells, resulting in the production of large amounts of immunoglobulins such as IgG, IgM, IgA, and IgE, and cytokines. Therefore, the IgE levels in Kawasaki disease are elevated.