Abstract
The Fc gamma receptor family contains several activating receptors and the only inhibitory receptor, FcγR2B. In this study, we investigated the dynamic methylation change of FcγR2B in different stages of Kawasaki disease (KD). We enrolled a total of 116 participants, which included patients with febrile diseases as controls and KD patients. Whole blood cells of KD patients were collected prior to intravenous immunoglobulin (IVIG) treatment (KD1), three to seven days after IVIG (KD2), three weeks after IVIG treatment (KD3), six months after IVIG (KD4), and one year after IVIG treatment (KD5). In total, 76 KD patients provided samples in every stage. Leukocytes of controls were also recruited. We performed DNA extraction and pyrosequencing. FcγR2B methylation levels were higher in KD3 compared to both the controls and KD1. A significantly higher methylation of FcγR2B was found in KD5 when compared with KD1. FcγR2B methylation levels in the IVIG-resistant group were lower than those in the IVIG-responsive group at KD1-3 (p = 0.004, 0.004, 0.005 respectively). This study is the first to report the dynamic change of FcγR2B methylation and to demonstrate long-term hypermethylation one year after disease onset. Hypomethylation of FcγR2B is associated with IVIG resistance.
Highlights
Kawasaki disease (KD) is a form of vasculitis characterized by such symptoms as conjunctivitis, strawberry tongue or erythema and cracking lips, skin rash, erythema and edema of the limbs, and cervical lymphadenopathy, in addition to a fever lasting at least five days, for the primary diagnostic criteria [1,2]
Of the 76 KD patients enrolled in this study, 18 had coronary artery aneurysms (CAAs)
We found no significant difference in FcγR2B methylation between KD patients and controls
Summary
Kawasaki disease (KD) is a form of vasculitis characterized by such symptoms as conjunctivitis, strawberry tongue or erythema and cracking lips, skin rash, erythema and edema of the limbs, and cervical lymphadenopathy, in addition to a fever lasting at least five days, for the primary diagnostic criteria [1,2]. An association between Fc receptors (FcR), inflammation, and KD has already been well-recognized [3,4]. FcγRIIB encoded by FcγR2B is the only inhibitory FcR and is expressed on neutrophils, eosinophils, mast cells, memory. Fc gamma receptors (FCGRs) play a vital role in mediating the inflammatory suppression by intravenous immunoglobulin (IVIG) through a Th2 pathway [7,8]. FcγRIIB expression on monocytes in KD patients with coronary artery aneurysms (CAAs) and the expression increased following IVIG treatment [7]. They observed that interleukin (IL)-6 and TNF-α mRNA in monocytes had a negative correlation with FcγRIIB expression on monocytes.
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