Key result
Adoptive transfer of concanavalin A-activated splenocytes from post-myocardial infarction rats into normal syngeneic rats produced cardiac-specific cellular infiltration and myocardial necrosis.
Why the study?
Does adoptive transfer of splenocytes from post-MI rats cause autoimmune myocarditis in normal syngeneic rats?
Population
Normal syngeneic rats
Design
Preclinical
Follow-up
6 weeks
Authors
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Supports T-cell autoimmunity in experimental post-MI injury; leaves open relevance to human HF progression.
Does adoptive transfer of splenocytes from post-MI rats cause autoimmune myocarditis in normal syngeneic rats?
This study provides direct in vivo evidence that myocardial infarction can trigger a T cell-mediated autoimmune response against cardiac antigens, potentially contributing to post-infarction heart failure progression.
Maisel et al. (1998) studied Myocardial infarction and autoimmune myocarditis. Adoptive transfer of concanavalin A-activated splenocytes from postinfarct rats was evaluated on Histopathological evidence of lymphocyte-mediated myocardial injury (infiltrate and necrosis). Adoptive transfer of concanavalin A-activated splenocytes from post-myocardial infarction rats into normal syngeneic rats produced cardiac-specific cellular infiltration and myocardial necrosis.
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