Association of mannose‐binding lectin gene polymorphisms with Kawasaki disease in the Japanese

Sato, Satoshi; Kawashima, Hisashi; Kashiwagi, Yasuyo; Fujioka, Tao; Takekuma, Kouji; Hoshika, Akinori

doi:10.1111/j.1756-185x.2009.01428.x

Cited by 16 publications

(10 citation statements)

References 18 publications

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“…While IgA is a weak activator of classical complement pathways, human polymeric serum IgA can bind to MBL, which activates the alternative lectin complement pathway (Roos et al, 2001). Furthermore, a polymorphism in MBL2 is an age-related risk factor for coronary artery lesions in KD patients (Biezeveld et al, 2003;Sato et al, 2009) and complement breakdown products C4d and C3d are upregulated in KD patients (Kohsaka et al, 1994). The finding that C3 deposits with IgA in LCWE-injected KD mice may indicate that these immune complexes contribute to inflammationdriven tissue injury and vessel damage.…”

Section: Discussionmentioning

confidence: 99%

Intestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation

et al. 2019

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Section: Discussionmentioning

confidence: 99%

Intestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation

et al. 2019

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“…In the acute stage of KD, there is sustained neutrophil activation [22], with increased release of human neutrophil elastase and matrix metalloproteinases [23], and similar patterns may be important in childhood asthma [24]. Polymorphisms in the mannose-binding lectin (MBL) gene have been reported to be associated with susceptibility to KD [25]. A role for MBL polymorphisms in susceptibility to asthma and allergic disease has also been reported [26].…”

Section: Discussionmentioning

confidence: 99%

Kawasaki disease and subsequent risk of allergic diseases: a population-based matched cohort study

et al. 2013

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BackgroundThe risk of allergic diseases among Kawasaki disease (KD) patients relative to the general population is not known. The aim of this study was to perform a population-based cohort study to investigate the risk of allergic diseases among children after KD in Taiwan- a country with the third highest incidence of KD in the world.MethodsData were obtained from the Taiwan National Health Insurance Research Database. In total, 253 patients who were 5 years of age or younger and had a first-time hospitalization with a diagnosis of KD between 1997 and 2005 were included as the study cohort and 1,012 non-KD patients matched for age and sex were included as comparison cohort. Multivariate Cox proportional hazard regression model was used to adjust for confounding and to compare the 6-year allergic-free survival rate between these two cohorts.ResultsThe incidence rate of allergic diseases (184.66 per 1000 person-year) was significantly higher in the KD cohort than in the control cohort (124.99 per 1000 person-years). After adjusting for potential confounders, the adjusted hazard ratios of asthma and allergic rhinitis were 1.51 (95% confidence interval = 1.17-1.95) and 1.30 (95% confidence interval = 1.04-1.62), respectively.ConclusionWe conclude that KD patients were at an increased risk for allergic diseases compared with the comparison cohort.

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“…Complement systems are rigorously regulated by more than ten protein species to prevent their undesirable excess activation. Genetic polymorphisms of these proteins might affect susceptibility of KD under infectious condition (106,112).…”

Section: Possible Implication Of Complement Pathwaysmentioning

confidence: 99%

Aetiological Significance of Infectious Stimuli in Kawasaki Disease

2019

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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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Association of mannose‐binding lectin gene polymorphisms with Kawasaki disease in the Japanese

Abstract: It is possible that mutations of the MBL gene might be related to the trigger of the pathogenesis of Kawasaki disease.

Cited by 16 publications

References 18 publications

Intestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation

Intestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation

Kawasaki disease and subsequent risk of allergic diseases: a population-based matched cohort study

Aetiological Significance of Infectious Stimuli in Kawasaki Disease

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