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Background  The main symptoms of Kawasaki disease (KD) are inflammatory vasculitis characterized by fever lasting 1–2 weeks, failure to respond to antibiotic treatment, conjunctivitis, redness of the lips and mouth, strawberry tongue, and painless enlargement of the neck lymph nodes. Studies have been shown that tumor necrosis factor (TNF) and TNF receptor family members are abnormally expressed in the acute phase of Kawasaki disease, also revealing that these two play a significant role in the pathogenesis of KD. The purpose of our study is to determine the relationship between  TNFRSF11A rs7239667  and the pathogenesis of KD and Coronary artery lesions in KD.    Methods and Results  In this study,  TNFRSF11A  ( rs7239667 ) genotyping was performed in 1396 patients with KD and 1673 healthy controls. Our results showed that  G  >  C  polymorphism of  TNFRSF11A  ( rs7239667 ) was not associated with KD susceptibility. In addition, the patients with KD were divided into CAA and NCAA groups according to whether they had coronary artery aneurysm (CAA) or not, and the  TNFRSF11A rs7239667  genotyping was performed in the two groups. After gender and age calibration, We found that genotype CC of  TNFRSF11A  may be a protective factor in KD coronary artery damage (adjusted OR = 0.69 95% CI = 0.49–0.99  P  = 0.0429) and is more significant in children with KD ≤ 60 months (adjusted OR = 0.49 95% CI = 0.49–0.93  P  = 0.0173).    Conclusion  Our study suggests that  TNFRSF11A rs7239667 G  >  C  polymorphism maybe play a protective gene role for the severity of KD coronary artery injury and is related to age, which has not been previously revealed.

Protective Effect of TNFRSF11A rs7239667 G > C Gene Polymorphism on Coronary Outcome of Kawasaki Disease in Southern Chinese Population