Journal
INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES
Volume 21, Issue 1, Pages 20-25Publisher
WILEY
DOI: 10.1111/1756-185X.13213
Keywords
acquired immune response; cytotoxic T lymphocytes; IgA; interferon; oligoclonal antibodies
Categories
Funding
- National Institute of Arthritis and Musculoskeletal and Skin Disease of the National Institutes of Health [R21AR068041]
- National Institute of Allergy and Infectious Diseases [R56AI106030]
- Max Goldenberg Foundation
- Center for Kawasaki Disease at the Ann & Robert H. Lurie Children's Hospital of Chicago
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R56AI106030] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R21AR068041] Funding Source: NIH RePORTER
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Although the etiology of Kawasaki disease (KD) is largely unknown, a large body of clinical, epidemiologic, immunologic, pathologic and ultrastructural evidence suggests that an infectious agent triggers a cascade that causes the illness. However, this elusive infectious agent remains unidentified at present. Increasingly sensitive molecular methods for identifying microbial nucleic acids and proteins in tissue samples continue to rapidly emerge, and these methods should be utilized in studies on KD etiology as they become available. Identifying the etiology of this enigmatic disease remains the single most important research goal in the field, and accomplishing this goal is the best means to improve diagnosis, treatment and prevention of this potentially fatal childhood disease.
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