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Isolation and Identification of Extravascular Immune Cells of the Heart
Published on: August 23, 2018
Role of IL-37- and IL-37-Treated Dendritic Cells in Acute Coronary Syndrome
Ruirui Zhu1, Fangyuan Zhang2, Chengliang Pan1
1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Insights
Interleukin-37 (IL-37) shows promise for treating acute coronary syndrome (ACS). This protein reduces inflammation and may offer a new therapeutic strategy for this common heart condition.
Area of Science:
- Cardiovascular Biology
- Immunology
- Inflammation Research
Background:
- Atherosclerosis, a chronic inflammatory disease, underlies acute coronary syndrome (ACS), a major cause of death and hospitalization.
- Understanding ACS mechanisms and identifying novel therapeutic targets are critical.
- Interleukin-37 (IL-37) is a natural inhibitor of innate and adaptive immunity, suppressing pro-inflammatory responses.
Purpose of the Study:
- To investigate the role and therapeutic potential of Interleukin-37 (IL-37) in acute coronary syndrome (ACS).
- To explore the immunomodulatory effects of IL-37 on dendritic cells (DCs) and their relevance to ACS.
Main Methods:
- Analysis of IL-37 levels in patients with ACS.
- Assessment of IL-37's effects on cardiac remodeling and ischemia/reperfusion injury in murine models.
- Evaluation of IL-37's impact on dendritic cell (DC) function and cytokine secretion.
Main Results:
- IL-37 levels were elevated and correlated with beneficial effects in patients with ACS.
- IL-37 treatment alleviated cardiac remodeling and myocardial ischemia/reperfusion injury in preclinical models.
- IL-37 induced tolerogenic properties in dendritic cells (DCs), characterized by increased immunosuppressive cytokine secretion.
Conclusions:
- IL-37 exhibits a protective role in ACS and may serve as a novel therapeutic agent.
- IL-37-modulated dendritic cells (tDCs) represent a potential cell-based therapy for ACS.
- Further research is warranted to elucidate the precise mechanisms of IL-37 action in ACS.
Abstract:
As a chronic inflammatory disease, atherosclerosis is a leading cause of morbidity and mortality in most countries. Inflammation is responsible for plaque instability and the subsequent onset of acute coronary syndrome (ACS), which is one of the leading causes of hospitalization. Therefore, exploring the potential mechanism underlying ACS is of considerable concern, and searching for alternative therapeutic targets is very urgent. Interleukin-37 (IL-37) inhibits the production of proinflammatory chemokines and cytokines and acts as a natural inhibitor of innate and adaptive immunity. Interestingly, our previous study with murine models showed that IL-37 alleviated cardiac remodeling and myocardial ischemia/reperfusion injury. Of note, our clinical study revealed that IL-37 is elevated and plays a beneficial role in patients with ACS. Moreover, dendritic cells (DCs) orchestrate both immunity and tolerance, and tolerogenic DCs (tDCs) are characterized by more secretion of immunosuppressive cytokines. As expected, IL-37-treated DCs are tolerogenic. Hence, we speculate that IL-37- or IL-37-treated DCs is a novel therapeutic possibility for ACS, and the precise mechanism of IL-37 requires further study.
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