Redness of the lips and mouth is the initial manifestation of oropharyngeal changes caused by cutaneous mucosal lymph node syndrome. Cutaneous mucosal lymph node syndrome, also known as Kawasaki disease (Kawasakisyndrome), is an acute systemic vasculitis with predominant onset in infants and children. The disease was first reported as cutaneous mucosal lymph node syndrome after cases with characteristic manifestations such as persistent fever, rash, and lymphadenitis, and what is the pathogenesis of Kawasaki disease? The etiology of Kawasaki disease is not yet clear, the disease is somewhat epidemic and landlord, clinical manifestations include fever, rash, etc., presumably related to infection, it is generally believed that a variety of pathogens, including EBV, retrovirus (retrovirus), or streptococcal, propionibacterium infection, in 1986 it was reported that the patient’s peripheral blood lymphocyte culture supernatant has increased reverse transcriptase activity, suggesting that the disease may be However, most studies have not obtained consistent results, and mycoplasma, rickettsia, and dust mites have been proposed as the etiology of the disease, but they have not been confirmed, and some people consider that environmental pollution or chemical allergy may be the cause of the disease. Recent studies have shown that there is an obvious immune dysregulation in the acute phase of the disease, which plays an important role in the pathogenesis of the disease, and the imbalance of peripheral blood T-cell subsets in the acute phase, with increased CD4, decreased CD8 and increased CD4/CD8 ratio. The increase in CD4/CD8 ratio puts the body’s immune system in an activated state, and CD4 secretes more lymphokines, which promote B-cell polyclonal water activation, proliferation and differentiation into plasma cells, resulting in elevated serum IgM, IgA, IgG, IgE, and high concentrations of interleukins (1L-1, 4, 5, 6), r-interferon (IFN-r), and tumor necrosis factor (TNF) from activated T-cells, all of which can induce endothelial cells to express and produce new These lymphokines and interferons can induce endothelial cells to express and produce new antigens; on the other hand, they also promote the secretion of autoantibodies by B cells, which leads to endothelial cell lysis cytotoxic effects and endothelial cell damage, so vasculitis occurs, 1L-11L-6, TNF increase can also induce hepatocytes to synthesize acute reactive proteins, such as C-reactive protein, αr-antitrypsin, binding bead protein, etc., causing acute febrile reactions in this disease. The mechanism of CIC in this disease is not clear, but there is no immune complex deposition at the lesion site, and serum C3 is elevated instead of decreased, which is not consistent with the general immune complex disease, the trigger cause of the above immune dysregulation is unknown, and nowadays it is believed that Kawasaki disease is a certain susceptible host triggered by a variety of infectious agents. It is now believed that Kawasaki disease is an immune-mediated systemic vasculitis triggered by a variety of infectious agents in the susceptible host.