Immunologic Studies of Heart Tissue: VI. Cardiac Lesions in Rabbits Associated with Autoantibodies to Heart Induced by Immunization with Heterologous Heart

MH Kaplan, JM Craig - The Journal of Immunology, 1963 - journals.aai.org
MH Kaplan, JM Craig
The Journal of Immunology, 1963journals.aai.org
Rabbits given repeated injections of beef or rat heart homogenates in aluminum hydroxide
gel adjuvant developed focal cardiac lesions associated with antibodies to heart. The
lesions were characterized by myocardial cell necrosis or degeneration with infiltration of
mononuclear and polymorphonuclear cells, among which eosinophils were frequently
prominent. Myocardial lesions of varying severity were observed in 7 of 9 animals injected
with beef heart and 6 of 12 animals injected with rat heart. An extensive myocardial …
Summary
Rabbits given repeated injections of beef or rat heart homogenates in aluminum hydroxide gel adjuvant developed focal cardiac lesions associated with antibodies to heart. The lesions were characterized by myocardial cell necrosis or degeneration with infiltration of mononuclear and polymorphonuclear cells, among which eosinophils were frequently prominent. Myocardial lesions of varying severity were observed in 7 of 9 animals injected with beef heart and 6 of 12 animals injected with rat heart. An extensive myocardial degeneration and fibrosis was observed rarely. In 13 control rabbits injected with human γ-globulin in adjuvant, these scattered focal lesions were not observed.
The incidence and severity of cardiac lesions could not be related to the titer of antibodies to heart as measured by complement fixation or immunofluorescence, or necessarily, to presence of flocculating antibodies.
Bound γ-globulin was detected within cardiac myofibers in focal sites of myocardium in several animals of the experimental groups, but not in the control animals. The sparseness of such deposits of bound γ-globulin in myocardium of most of the experimental animals, despite the presence of circulating antibodies to heart, suggested that impermeability of myofibers to antibody may represent a limiting factor in the pathogenesis of these lesions.
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