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The Journal of Immunology, 1999, 163: 1060-1065.
Copyright © 1999 by The American Association of Immunologists

Anti-Human Cardiac Myosin Autoantibodies in Kawasaki Syndrome1

Madeleine W. Cunningham*, H. Cody Meissner{dagger}, Janet S. Heuser*, Biagio A. Pietra§, David K. Kurahara{ddagger} and Donald Y. M. Leung2

* Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190; {dagger} Department of Pediatrics, New England Medical Center, Boston, MA 02111; {ddagger} Department of Tropical Medicine and Medical Microbiology, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96822; § Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO 80262; and Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206

Kawasaki syndrome (KS) is the major cause of acquired heart disease in children. Although acute myocarditis is observed in most patients with KS, its pathogenesis is unknown. Because antimyosin autoantibodies are present in autoimmune myocarditis and rheumatic carditis, the purpose of the current study was to determine whether anticardiac myosin Abs might be present during the acute stage of KS. Sera from KS patients as well as age-matched febrile controls and normal adults were compared for reactivity with human cardiac myosin in ELISAs and Western blot assays. A total of 5 of 13 KS sera, as compared with 5 of 8 acute rheumatic fever sera, contained Ab titers to human cardiac myosin that were significantly higher than those found in control sera. Both cardiac and skeletal myosins were recognized in the ELISA by KS sera, although stronger reactivity was observed to human cardiac myosin. Only IgM antimyosin Abs from KS sera were significantly elevated relative to control sera. KS sera containing antimyosin Abs recognized synthetic peptides from the light meromyosin region of the human cardiac myosin molecule and had a different pattern of reactivity than acute rheumatic fever sera, further supporting the association of antimyosin Ab with KS. These Abs may contribute to the pathogenesis of acute myocarditis found in patients with KS.




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