Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 222, Issue 1, Pages 158-168Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiaa066
Keywords
plasmablast; monoclonal antibodies; Kawasaki disease
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Funding
- National Institute of Allergy and Infectious Diseases [R21 AI140029]
- Office of the Director Shared Instrument Grant [1S10OD011996-01]
- Feitler Family
- Max Goldenberg Foundation
- Center for Kawasaki Disease at the Ann
- Robert H. Lurie Children's Hospital of Chicago
- National Cancer Institute [P30 CA060553]
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Background. Kawasaki disease (KD) is the leading cause of childhood acquired heart disease in developed nations and can result in coronary artery aneurysms and death. Clinical and epidemiologic features implicate an infectious cause but specific antigenic targets of the disease are unknown. Peripheral blood plasmablasts are normally highly clonally diverse but the antibodies they encode are approximately 70% antigen-specific 1-2 weeks after infection. Methods. We isolated single peripheral blood plasmablasts from children with KD 1-3 weeks after onset and prepared 60 monoclonal antibodies (mAbs). We used the mAbs to identify their target antigens and assessed serologic response among KD patients and controls to specific antigen. Results. Thirty-two mAbs from 9 of 11 patients recognize antigen within intracytoplasmic inclusion bodies in ciliated bronchial epithelial cells of fatal cases. Five of these mAbs, from 3 patients with coronary aneurysms, recognize a specific peptide, which blocks binding to inclusion bodies. Sera from 5/8 KD patients day >= 8 after illness onset, compared with 0/17 infant controls (P < .01), recognized the KD peptide antigen. Conclusions. These results identify a protein epitope targeted by the antibody response to KD and provide a means to elucidate the pathogenesis of this important worldwide pediatric problem.
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