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Monoclonal Antibodies From Children With Acute Kawasaki Disease Identify a Common Antigenic Target in Fatal Cases
Anne H Rowley1, Robert Byrd2, David Arrollo3
1Department of Pediatrics, Northwestern University Feinberg School of Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois; Department of Microbiology/Immunology, Northwestern University Feinberg School of Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
Insights
Researchers identified intracytoplasmic inclusion bodies in Kawasaki disease (KD) patients
Area of Science:
- Pediatric Infectious Diseases
- Immunology
- Pathogen Discovery
Background:
- Kawasaki disease (KD) is a critical febrile illness in children, potentially leading to severe cardiac complications like coronary artery aneurysms.
- Epidemiological patterns suggest an infectious agent, possibly transmitted via respiratory routes, yet no definitive pathogen has been identified.
- Previous research indicated intracytoplasmic inclusion (ICI) bodies in KD bronchial epithelium and a specific antibody response, hinting at a respiratory causative agent.
Purpose of the Study:
- To investigate the presence and significance of intracytoplasmic inclusion (ICI) bodies in Kawasaki disease (KD) patients.
- To confirm a predominant respiratory causative agent for KD using expanded monoclonal antibodies.
- To assess the geographic and temporal prevalence of the identified KD agent.
Main Methods:
- Immunohistochemistry and epitope binding assays were performed on bronchial epithelium samples from KD patients and controls.
- An expanded panel of monoclonal antibodies, derived from plasmablasts of children with acute KD, was utilized.
- ICI bodies were detected using a representative monoclonal antibody in fatal KD cases across five decades and diverse geographic locations.
Main Results:
- Monoclonal antibodies from all 12 acute KD patients recognized ICI bodies in bronchial epithelium.
- ICI bodies were present in 100% (20/20) of fatal KD cases from the US and Japan spanning 50 years.
- ICI bodies were absent in 95% (19/20) of infant controls, demonstrating high specificity.
Conclusions:
- The consistent presence of ICI bodies across decades and geographies strongly supports a single, predominant causative agent for Kawasaki disease (KD).
- These findings validate the role of ICI bodies as a key marker for KD etiology.
- Future research should focus on identifying the specific infectious agent responsible for KD, guided by these findings.
Abstract:
Kawasaki disease (KD) is a unique febrile illness of young children that can result in coronary artery aneurysms, myocardial infarction, aneurysm rupture, and sudden death. The epidemiologic features, including the young age group affected, the rarity of recurrence, and the presence of epidemics and outbreaks, point to a single infectious causative agent. The recent decrease in KD cases worldwide during pandemic mitigation supports transmission of the agent via a respiratory route. However, substantial research over decades has shown that KD etiology cannot be linked to any currently known infectious agent. We previously identified the presence of intracytoplasmic inclusion (ICI) bodies in the bronchial epithelium in children with fatal KD and a convergent plasmablast-derived antibody response to a specific protein epitope, supporting 1 predominant respiratory causative agent. Here, we report immunohistochemistry and epitope binding using an expanded pool of KD monoclonal antibodies prepared from single peripheral blood plasmablasts from 12 children with acute KD. We identified 1 or more monoclonal antibodies from each of the 12 patients that recognized ICI bodies in KD bronchial epithelium. Using a representative monoclonal antibody, ICI bodies were detected in 20 of 20 children with fatal KD across 5 decades, 10 from the United States and 10 from Japan, and were absent in 19 of 20 infant controls (P < .001). We also found that all 12 children with acute KD generated plasmablast(s) recognizing the previously reported peptide antigen. Taken together, these results point to 1 predominant causative agent of KD across many decades and geographic areas and should direct future KD research studies.
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