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Published on: March 1, 2024
Aetiological Significance of Infectious Stimuli in Kawasaki Disease
Akihiro Nakamura1, Kazuyuki Ikeda2, Kenji Hamaoka3,4
1Central Research Laboratory, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Insights
Kawasaki disease (KD) pathogenesis involves immune dysregulation triggered by infections. This review explores viral, bacterial, and innate immune responses, plus genetic factors, in KD development.
Area of Science:
- Pediatric rheumatology
- Immunology
- Infectious diseases
Background:
- Kawasaki disease (KD) is a critical pediatric vasculitis characterized by coronary artery abnormalities.
- The exact causes and pathogenesis of KD remain incompletely understood.
- Existing evidence links KD pathogenesis to aberrant immune responses against infectious agents.
Purpose of the Study:
- To review the role of infectious stimuli in Kawasaki disease etiology.
- To explore the interplay between immune responses, pathogens, and genetic predisposition in KD.
Main Methods:
- Review of clinical and experimental evidence regarding KD.
- Analysis of the immune response to viral and bacterial infections.
- Examination of innate immune pathways and genetic influences in KD.
Main Results:
- Viral infections are implicated in KD pathogenesis.
- Bacterial infections and superantigen hypotheses are considered.
- Innate immunity, including PAMPs and complement, plays a role.
- Genetic background influences immune responses to infectious triggers.
Conclusions:
- A diverse range of microbes and viruses may trigger KD.
- Common and distinct immune pathways are involved in KD development.
- Understanding these immune processes is crucial for elucidating KD etiology.
Abstract:
Kawasaki disease (KD) is a pediatric vasculitis syndrome that is often involves coronary artery lesions (e. g., coronary artery aneurysms). Although its causal factors and entire pathogenesis remain elusive, the available evidence indicates that the pathogenesis of KD is closely associated with dysregulation of immune responses to various viruses or microbes. In this short review, we address several essential aspects of the etiology of KD with respect to the immune response to infectious stimuli: 1) the role of viral infections, 2) the role of bacterial infections and the superantigen hypothesis, 3) involvement of innate immune response including pathogens/microbe-associated molecular patterns and complement pathways, and 4) the influence of genetic background on the response to infectious stimuli. Based on the clinical and experimental evidence, we discuss the possibility that a wide range of microbes and viruses could cause KD through common and distinct immune processes.
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