Mucocutaneous lymph node syndrome (MCLS), also known as Kawasaki disease, is an acute febrile rash pediatric disease characterized by systemic vasculitis. The disease has attracted attention because of the serious cardiovascular lesions that can occur. Mucocutaneousmphnodesyndrome (MCLS), also known as Kawasakidisease, is an acute febrile rash pediatric disease characterized by systemic vasculitis, first reported by Dr. Tomisaku Kawasaki in 1967. As this disease can occur serious cardiovascular pathology, people pay attention to the increase in the incidence of recent years, in 1990, Beijing Children’s Hospital rheumatic disease inpatient cases, Kawasaki disease 67 cases, rheumatic fever 27 cases; 11 hospitals in foreign provinces and cities the same information, Kawasaki disease for rheumatic 2 times. Apparently Kawasaki disease has replaced rheumatic fever as one of the main causes of pediatric acquired heart disease in China. Kawasaki disease is now considered to be an immune-mediated vasculitis and is temporarily coded within the connective tissue diseases chapter. The etiology of severe red congestion of the mouth and lips: The disease is somewhat epidemic and landlord, with clinical manifestations such as fever and rash, presumably related to infection. In 1986, an increase in reverse transcriptase activity in peripheral blood lymphocyte culture supernatants was reported, suggesting that the disease may be caused by a retrovirus. However, most studies have not obtained consistent results. Mycoplasma, rickettsia, and dust mites have also been proposed as the etiologic agent of the disease, but this has not been confirmed. Environmental pollution or chemical allergy has also been considered as a possible cause of the disease. Recent studies have shown that there is a significant immune dysregulation in the acute phase of the disease, which plays an important role in the pathogenesis. There is an imbalance of peripheral blood T-cell subsets in the acute phase, with an increase in CD4, a decrease in CD8, and an increase in the CD4/CD8 ratio. The increased CD4/CD8 ratio puts the body’s immune system in an activated state and increases the secretion of lymphokines by CD4, which promotes the activation, proliferation and differentiation of B-cell polyclonal water into plasma cells, leading to an increase in serum IgM, IgA, IgG and IgE, and the secretion of high concentrations of interleukins (1L-1, 4, 5, 6), r , 5, 6), r-interferon (IFN-r), and tumor necrosis factor (TNF). These lymphokines and active interferons can induce endothelial cells to express and produce neoantigens, and on the other hand promote B cells to secrete autoantibodies, which leads to endothelial cell lysis cytotoxic effects and endothelial cell damage so vasculitis occurs. 1L-11L-6 and TNF increase can also induce hepatocytes to synthesize acute reactive proteins, such as C-reactive protein, αr-antitrypsin, binding bead protein, etc. This causes an acute febrile response to the disease. The mechanism of the role of CIC in this disease is not clear, but the absence of immune complex deposits at the lesion site and the increase in serum C3 instead of decreasing are not consistent with general immune complex disease. The trigger cause of these immune dysregulation is unknown. Kawasaki disease is nowadays considered to be an immune-mediated systemic vasculitis triggered by a variety of infectious agents in a certain susceptible host.