Kawasaki disease, also known as cutaneous mucocutaneous lymph node syndrome, is an acute febrile rash disease that occurs mainly in infants and young children under the age of 5 years, and is associated with generalized vasculitis at the time of onset of the disease, so it belongs to the vasculitis syndrome. Since 1967, when it was first reported by Japanese doctor Tomisaku Kawasaki, the disease has been reported worldwide. Epidemiological studies in Japan, the United States, Canada, Taiwan and Beijing have shown that the incidence of the disease has been increasing year by year, and it has become the main cause of acquired heart disease in children in North America and Japan, and it is also one of the common cardiovascular diseases in pediatrics in China. I. Etiology and pathogenesis The etiology of Kawasaki disease is still unclear, but clinical and epidemiologic data support that the etiology of the disease may be infectious factors. First, the five main clinical manifestations of the disease, fever, rash, redness and swelling of the palms of the hands, and conjunctival congestion, are all similar to infectious diseases, and are sometimes more difficult to distinguish from infectious diseases such as adenoviral infections and scarlet fever, which are markedly self-limiting and have a very low rate of recurrence, which supports infectious diseases; second, there is a clear winter/spring peak of onset of the disease in most areas; third, there is a distinct place of onset for each epidemic; and fourth, there is an age peaks of incidence, both more in infants and young children, and less in adults and pediatrics under 3 months of age support what appears to be an antibody that can pass through the placenta at work, with pediatric infants getting antibodies from their mothers, and adults mostly immune because of occult infections. However, many scholars have screened for evidence of infection with a myriad of microorganisms over the last 30 years or so, but have so far failed to obtain positive results. Initially, standard bacteria and viruses were used to fail to isolate the relevant pathogens from the body fluids of affected children, and inoculation of animals with body fluids from affected children failed to replicate the disease. Subsequent attempts to detect pathogen-associated nucleic acids from patients with lung disease or recovering children using modern molecular techniques have also failed to yield positive results. Recent studies have focused on the role of bacterial toxins as a superantigen that induces an autoimmune response in the body leading to the disease, but the results are still highly controversial; some studies have been supported by positive results, finding elevated levels of Vβ-T cell receptors in peripheral blood of children with Kawasaki disease, which may be related to the superantigenic pathogenesis, but other studies have been unable to reproduce these results. Some studies have shown that children with Kawasaki disease have different lymphocyte turnover than normal controls, suggesting that immunity is involved in the pathogenesis of the disease. Because Kawasaki disease is significantly more prevalent in Asian populations than in Caucasian populations, it has been hypothesized that the disease may be genetically related, but to date, certain human leukocyte-associated antigens, among others, have not been found to be associated with the disease. Some scholars have studied the immunoglobulin-associated antigens of children of different races with Kawasaki disease, suggesting that certain genes are more prevalent in the Japanese population than in the Caucasian population, suggesting that immunoglobulin genes seem to predispose Asian populations to the risk of developing the disease. Recently there have been attempts to find the cause of the disease by first finding a biochemical marker to diagnose the disease by that route. This idea was inspired by the discovery of the E-B virus, where a way to diagnose the infection was first found before humans discovered the E-B virus, which was the heterophilic agglutination test, and subsequently isolated the virus. If such a biochemical marker could be found in children with Kawasaki disease, it would not only facilitate the discovery of the cause of the disease, but also the early treatment of the disease. In fact, some scholars have been experimenting whether a metalloproteinase can specifically diagnose the disease, and the results have yet to be proved. Second, pathological changes Pathological examination of the dead cases revealed that the pathological changes of Kawasaki disease were mainly manifested as systemic nonspecific vascular inflammation, and the course of the disease could be divided into four stages48,49: the first stage (0-9 days), characterized by periarteritis of the small arteries, which could be seen as pericarditis, myocarditis, endocarditis, inflammation of the cardiac valves, and inflammation of the atrioventricular conduction system; the second stage (12-25 days), characterized by medium-sized have Total vasculitis with aneurysm formation and thrombus in medium-sized myocardial arteries; pericarditis, myocarditis, endocarditis, and valvular inflammation can also be seen in this stage; in the third stage (28-31 days), endothelial hyperplasia of coronary and other medium-sized arteries is manifested, and acute inflammatory reaction in the vessel wall subsides; in the fourth stage (after 40 days), endothelial plaque formation in the arteries and partial stenosis of the blood vessels can be seen. Vasculitis in Kawasaki disease is related to the body’s immune regulatory system, and Leung et al. first found a decrease in circulating CD8+ suppressor/cytotoxic T cells and an increase in circulating activated B cells that spontaneously produce immunoglobulins in children with Kawasaki disease.50 Furukawa et al.51,52 found that peripheral blood mononuclear cells were activated in the acute phase of the pathogenesis, and that a large number of inflammatory cytokines activated in the immune system53- 55 that are involved in the pathogenesis of arteritis. Some studies have demonstrated that the activation of cellular inflammatory factors is genetically mediated, which may explain the different prevalence in different populations56,57.