Why the study?
A balanced and timely terminated proinflammatory response following acute MI is essential for tissue repair and regeneration, but the underlying regulatory mechanisms are poorly defined.
Do IL-10-producing B cells facilitate resolution of inflammation and reduce myocardial injury after acute myocardial infarction in mice?
Do IL-10-producing B cells facilitate resolution of inflammation and reduce myocardial injury after acute myocardial infarction in mice?
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IL-10-producing B cells in pericardial adipose tissues play a protective role after acute myocardial infarction by resolving inflammation and preserving cardiac function, identifying them as potential therapeutic targets.
Significance Myocardial infarction (MI) remains a leading cause of mortality and morbidity worldwide. Although it is recognized that a balanced and timely terminated proinflammatory response following acute MI is essential in promoting tissue repair/regeneration, the underlying regulatory mechanisms are poorly defined. In this report, we show that IL-10–producing B cells in mice: 1) Are enriched in pericardial adipose tissues (PATs) and influenced by cytokines preferentially expressed in these tissues; 2) expand in PATs following MI and accumulate in the infarcted heart during the resolution of MI-induced inflammation; and 3) facilitate resolution of inflammation and reduce myocardial injury to preserve cardiac function after MI. These findings identify IL-10–producing B cells, in particular those in PATs, as therapeutic targets for MI.
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Wu et al. (2019) studied this question.
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