Key result
PD1 depletion before reperfused murine AMI fails to reduce infarct size but increases CD8+ T cells.
Why the study?
Understanding the relevance of cardiac PD1 signaling may provide new insights into inflammatory events under baseline conditions and disease.
Does PD1 deficiency or depletion modify cardiac immunity and infarct size in baseline conditions and reperfused acute myocardial infarction?
Population
Mice under baseline conditions and in a reperfused acute myocardial infarction model
Comparison
PD1 deficiency or pharmacological depletion vs controls
Design
Preclinical animal study
Authors
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Does not support PD1 depletion to limit infarct size; leaves open the role of CD8+ T cells in murine post-MI remodeling.
Does PD1 deficiency or depletion modify cardiac immunity and infarct size in baseline conditions and reperfused acute myocardial infarction?
PD1/PDL1 signaling plays a significant role in cardiac immunity, highlighting potential risks for adverse outcomes from acute myocardial infarction in patients receiving immune checkpoint inhibitors.
Michel et al. (2022) studied Reperfused acute myocardial infarction (repAMI). PD1 deficiency and pharmacological depletion of PD1 vs. Baseline conditions / untreated mice was evaluated on Area of infarction and inflammatory changes (CD8+ T cells). Pharmacological depletion of PD1 prior to reperfused acute myocardial infarction in mice did not alter the area of infarction but led to increased numbers of CD8+ T cells.
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