Circulation, Vol 85, 1918-1926, Copyright © 1992 by American Heart Association
M Kodama, Y Matsumoto and M Fujiwara
BACKGROUND. To elucidate the mechanisms of immune-related myocardial
injuries, we examined whether autoimmune myocarditis was passively
transferable by use of humoral or cellular factors. METHODS AND RESULTS.
Active myocarditis was elicited in Lewis rats by immunization with human
cardiac myosin fraction in complete Freund's adjuvant. This experimental
myocarditis was characterized by macroscopic features such as pericardial
effusion, enlargement of the heart, and gray discoloration of the cardiac
surface. Histologically, extensive myocardial necrosis and numerous
inflammatory cell infiltrations were observed. Interestingly,
multinucleated giant cells were frequently observed in the lesions.
Transfer of the disease by the humoral factor was examined by use of fresh
sera and immunoglobulin fraction of pooled sera from rats with severe
myocarditis, and transfer by the cellular factor was tested by use of
spleen cells and lymph node cells from the diseased rats. When naive Lewis
rats were given 15.75 mg of immunoglobulin fraction, no particular change
was observed in the hearts. Fresh sera also could not elicit myocarditis in
recipient rats. In contrast, intravenous injection of spleen cells or lymph
node cells that were cultured for 3 days in the presence of 1 microgram/ml
of concanavalin A elicited severe myocarditis. The macroscopic and
microscopic findings of passively transferred myocarditis are essentially
the same as those found in actively induced myocarditis. Multinucleated
giant cells were also observed in the lesions of transferred myocarditis.
CONCLUSIONS. This study demonstrates direct evidence for in vivo
lymphocyte-mediated myocardial injuries.
ARTICLES
In vivo lymphocyte-mediated myocardial injuries demonstrated by adoptive transfer of experimental autoimmune myocarditis
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
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