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Published on: August 17, 2022
HMGB1 blockade attenuates experimental autoimmune myocarditis and suppresses Th17-cell expansion
Zhaoliang Su1, Caixia Sun, Chenglin Zhou
1Department of Immunology, Jiangsu University, Zhenjiang, PR China.
Insights
Blocking High-mobility group box 1 (HMGB1) with an antibody reduced inflammation and heart damage in experimental autoimmune myocarditis. This approach suppressed Th17 cells, suggesting a new therapeutic strategy for heart failure.
Area of Science:
- Immunology
- Cardiology
- Molecular Biology
Background:
- High-mobility group box 1 (HMGB1) is a nuclear protein linked to cardiovascular diseases.
- Dilated cardiomyopathy (DCM) often results from coxsackievirus B3-induced myocarditis and autoimmune processes.
- Th17 cells, a CD4+ T cell subset, play a role in autoimmune myocarditis pathogenesis.
Purpose of the Study:
- To investigate the effects of blocking HMGB1 function on Th17 cells and experimental autoimmune myocarditis (EAM).
- To assess the therapeutic potential of anti-HMGB1 B box monoclonal antibody (mAb) in EAM.
Main Methods:
- Induction of EAM in a study model.
- Administration of an anti-HMGB1 B box mAb.
- Measurement of HMGB1 levels, cardiac pathology, inflammatory cell infiltration, Th17 cell counts, and IL-17 levels.
- In vitro studies on HMGB1's effect on Th17 cell expansion.
Main Results:
- HMGB1 protein levels were elevated in the heart and blood during EAM.
- Anti-HMGB1 B box mAb treatment attenuated cardiac pathology and reduced inflammatory cell infiltration.
- HMGB1 blockade correlated with decreased Th17 cells and lower serum IL-17 levels.
- In vitro, HMGB1 was found to promote Th17 cell expansion.
Conclusions:
- HMGB1 blockade ameliorates cardiac pathological changes in EAM.
- Suppression of Th17 cells is a key mechanism underlying the protective effects of HMGB1 blockade.
- Targeting HMGB1 may offer a novel therapeutic strategy for autoimmune myocarditis and related heart conditions.
Abstract:
High-mobility group box 1 (HMGB1), a non-histone nuclear protein, has been implicated in cardiovascular diseases. Dilated cardiomyopathy (DCM), one of the leading causes of heart failure, is often caused by coxsackievirus B3-triggered myocarditis and promoted by the post-infectious autoimmune process. Th17 cells, a novel CD4(+) T subset, may be important in the pathogenesis of autoimmune myocarditis. In the present study, we attempted to block HMGB1 function with a monoclonal antibody specific for HMGB1 B box and investigated the effects of the blockade on Th17 cells and experimental autoimmune myocarditis (EAM). After induction of EAM, HMGB1 protein levels were significantly elevated both in the heart and blood. Administration of an anti-HMGB1 B box mAb attenuated cardiac pathological changes and reduced the number of infiltrating inflammatory cells in the heart during EAM. These protective effects of HMGB1 blockade correlated with a reduced number of Th17 cells in local tissues and lower levels of IL-17 in the serum. Furthermore, in vitro, studies demonstrated that HMGB1 promoted Th17-cell expansion. Therefore, we speculate that HMGB1 blockade ameliorates cardiac pathological changes in EAM by suppressing Th17 cells.
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