TWEAK and CD163 expression in dendritic cells and macrophages may promote an inflammatory milieu after STEMI, potentially contributing to adverse remodeling and heart failure.
The activation of the innate immune system is crucial for myocardial recovery after acute myocardial infarction (AMI). Dendritic cells (DCs) and macrophages regulate inflammation and healing of the ischemic heart. This study aims to evaluate the levels of DCs and macrophages expressing CD163 and TWEAK in patients with acute ST-elevation myocardial infarction (STEMI). We decided to evaluate the frequency of CD163+ TWEAK+ DCs and macrophages in patients with STEMI within the first 72 h, as well as at 3 and 6 months after the acute event. We observed that expression of CD163 and TWEAK in myeloid DCs was higher in STEMI patients at 3-month follow-up, and this was associated with worse cardiac function. sTWEAK levels were higher in STEMI patients within 72 h after AMI and positively correlated with a better left ventricular ejection fraction (LVEF). Finally, in M2 Macrophages, rh-TWEAK administration resulted in a dose-dependent decrease in CD163 expression. mDC, pDC, as well as M1/M2 macrophages express CD163 and TWEAK. ages. Our results indicate that TWEAK and CD163 may be promoting an inflammatory milieu after AMI. Thus, an imbalance in the expression of these molecules can then lead to chronic inflammation, tissue damage, and heart failure.
Sherell et al. (Sun,) studied this question.