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,
Departments of
*
Pediatrics and
Microbiology and Immunology, Northwestern University Medical School, Chicago, IL 60611;
Children’s Memorial Hospital, Chicago, IL 60614; and
Department of Microbiology and Immunology, Loyola University Stritch School of Medicine, Maywood, IL 60153
The costs of publication of this article were defrayed in part by
the payment of page charges. This article must therefore be hereby
marked advertisement in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Kawasaki Disease (KD) is a potentially fatal acute vasculitis of
childhood. Although KD is the leading cause of acquired heart disease
in children in developed nations, its pathogenesis remains unknown. We
previously reported the novel observation that IgA plasma cells
infiltrate the vascular wall in acute KD. We have now examined the
clonality of this IgA response in vascular tissue from three fatal
cases of KD to determine whether it is oligoclonal, suggesting an
Ag-driven process, or polyclonal, suggesting nonspecific B cell
activation or a response to a superantigen. We first sequenced VDJ
junctions of 44 
genes isolated from a primary, unamplified KD
vascular cDNA library. Five sets of clonally related sequences were
identified, comprising 34% (15 of 44) of the isolated sequences.
Furthermore, point mutations consistent with somatic mutation were
detected in the related sequences. Next, using formalin-fixed coronary
arteries from two additional fatal KD cases, we sequenced VDJ junctions
of genes isolated by RT-PCR, and a restricted pattern of CDR3 usage
was observed in both. We conclude that the vascular IgA response in
acute KD is oligoclonal. The identification of an oligoclonal IgA
response in KD strongly suggests that the immune response to this
important childhood illness is Ag-driven.
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