CD100 modulates cytotoxicity of CD8+ T cells in patients with acute myocardial infarction

BMC Immunology

Kunpeng Song¹  Li Qin¹  Jingjing Zhang¹  Ruixue Chen¹  Yan Li¹  Qijun Bai¹ 

[1] Department of Cardiovascular Medicine Ward II, Zhengzhou Central Hospital Affiliated to Zhengzhou University;

关键词: Acute myocardial infarction;    CD100;    T lymphocytes;    Immunoregulation;   

DOI  :  10.1186/s12865-021-00406-y

来源: DOAJ

【 摘 要 】

Abstract Background CD100 is an immune semaphorin family member that highly expressed on T cells, which take part in the development of acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) are important mediators for membrane-bound CD100 (mCD100) shedding from T cells to generate soluble CD100 (sCD100), which has immunoregulatory effect on T cells. The aim of this study was to investigate modulatory role of CD100 on CD8+ T cell activity in AMI patients. Methods Peripheral sCD100 and MMP-2 level, as well as mCD100 level on T cells was assessed in patients with stable angina pectoris (SAP), unstable angina pectoris (UAP), and AMI. The regulatory function of MMP-2 on mCD100 shedding, sCD100 formation, and cytotoxicity of CD8+ T cells was analyzed in direct and indirect contact co-culture system. Results AMI patients had higher peripheral sCD100 and lower mCD100 expression on CD8+ T cells in comparison with SAP, UAP, and controls. CD8+ T cells in AMI patients showed elevated direct cytotoxicity, enhanced cytokine production, and increased perforin/granzyme B secretion. Recombinant sCD100 stimulation promoted cytolytic function of CD8+ T cells in controls and AMI patients. Furthermore, AMI patients also had elevated circulating MMP-2 level. Recombinant MMP-2 stimulation induced mCD100 shedding from CD8+ T cells and sCD100 generation, resulting in enhancement of CD8+ T cell cytotoxicity in AMI patients. Conclusion Up-regulation of MMP-2 might contribute to elevation of mCD100 shedding and sCD100 formation, leading to increased cytotoxicity CD8+ T cells in AMI patients.

【 授权许可】

Unknown