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Identification of increased expression of activating Fc receptors and novel findings regarding distinct IgE and IgM receptors in Kawasaki disease

  • Ling Sai Chang
  • , Mindy Ming-Huey Guo
  • , Mao Hung Lo
  • , Ho Chang Kuo*
  • *Corresponding author for this work
  • Chang Gung University
  • Chang Gung Memorial Hospital

Research output: Contribution to journalJournal Article peer-review

23 Scopus citations

Abstract

Background: Kawasaki disease (KD) is associated with expression and methylation of Fc gamma receptor genes. We characterized immunoglobulin A (IgA), IgE, IgG, and IgM receptor expression levels in KD. Methods: Fc receptor expression levels were characterized using GeneChip Human Transcriptome Array 2.0 (HTA 2.0) with 18 KD patients, 18 non-febrile controls, and 18 febrile controls. Another 48 control individuals and 46 patients with KD were measured using pyrosequencing for the methylation levels. Results: The mRNA expression levels of FCER1A and FCER2 were significantly lower in KD patients than in non-febrile controls and then rose following treatments with intravenous immunoglobulin (IVIG). Expression levels of FCER1G increased compared to the non-febrile subjects and then subsided after IVIG. FCER1A methylation was significantly lower among KD patients and even lower in KD patients with IVIG resistance. HTA analysis revealed higher mRNA levels of FCAR, FCGR1C, and FCGR2A in KD patients. FCMR mRNA expression levels were significantly lower in KD patients. FCMR expression levels rose after IVIG treatment. After IVIG, FCGR1A, B, and C decreased even lower than the febrile controls. Conclusion: This is the first study indicating that IgA, IgE, IgG, and IgM receptors are associated with KD. We highlighted potential biomarkers related to Fc receptors and their regulation.

Original languageEnglish
Pages (from-to)191-197
Number of pages7
JournalPediatric Research
Volume89
Issue number1
DOIs
StatePublished - 01 2021

Bibliographical note

Publisher Copyright:
© 2019, International Pediatric Research Foundation, Inc.

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