DC-SIGN (CD209) promoter -336 A/G (rs4804803) polymorphism associated with susceptibility of Kawasaki disease.

Kawasaki disease (KD) is characterized by systemic vasculitis of unknown etiology. High-dose intravenous immunoglobulin (IVIG) is the most effective therapy for KD to reduce the prevalence of coronary artery lesion (CAL) formation. Recently, the α2, 6 sialylated IgG was reported to interact with a lectin receptor, specific intracellular adhesion molecule-3 grabbing nonintegrin homolog-related 1 (SIGN-R1) in mice and dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) in human, and to trigger an anti-inflammatory cascade.

Polymorphisms of transforming growth factor-β signaling pathway and Kawasaki disease in the Taiwanese population.

Kawasaki disease (KD) is a systemic vasculitis associated with cardiovascular symptom. A previous study in the European descent has indicated that genetic variants of the transforming growth factor-β (TGF-β) pathway are involved in the KD susceptibility and clinical status. This study was conducted to investigate if polymorphisms in TGF-β signaling pathway are associated with KD susceptibility, and the coronary artery lesion formation.

[Atypical kawasaki disease: literature review and clinical nursing].

Kawasaki disease (KD) is an acute febrile multi-systemic vasculitis of unknown etiology that primarily affects children under 5 years of age. KD has been singled out as a main cause of acquired childhood heart disease. Its etiology, genetic background, and immunopathogenesis remain unclear.