• 国家药监局综合司 国家卫生健康委办公厅
  • 国家药监局综合司 国家卫生健康委办公厅

[title missed]

Corresponding author: HE kai
DOI: 10.12201/bmr.202510.00016
Statement: This article is a preprint and has not been peer-reviewed. It reports new research that has yet to be evaluated and so should not be used to guide clinical practice.
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    Abstract: Kawasaki disease is an acute systemic vasculitis mainly affecting children under 5 years old, and has become the leading cause of acquired heart disease in children. The etiology is not yet fully understood, and it is generally believed to be caused by abnormal immune responses triggered by infectious factors in genetically susceptible individuals. In recent years, studies have shown that polymorphisms in multiple genes such as ITPKC and CASP3 are associated with disease susceptibility and risk of coronary artery disease; Multiple pathogens such as Staphylococcus aureus, influenza virus, adenovirus, etc. may induce immune responses through mechanisms such as superantigen activation and molecular mimicry; In terms of immune mechanism, the formation of neutrophil extracellular traps (NETs), imbalance of T cell subsets, and abnormal activation of B cells jointly promote the occurrence and development of vascular inflammation. This article systematically reviews the new progress in the etiology and pathogenesis of Kawasaki disease in terms of genetics, infection, and immunity, in order to provide theoretical basis for early diagnosis, risk warning, and treatment of the disease.

    Key words: Kawasaki disease; pathogeny; Pathogenesis; Genetic susceptibility; Infection factors; immune activation

    Submit time: 11 October 2025

    Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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  • ID Submit time Number Download
    1 2025-09-05

    bmr.202510.00016V1

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张亚, HE kai. [title missed]. 2025. biomedRxiv.202510.00016

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