دورية أكاديمية
Inhibitor of CD147 Suppresses T Cell Activation and Recruitment in CVB3-Induced Acute Viral Myocarditis
العنوان: | Inhibitor of CD147 Suppresses T Cell Activation and Recruitment in CVB3-Induced Acute Viral Myocarditis |
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المؤلفون: | Ruifang Wang, Kexin Zong, Juan Song, Qinqin Song, Dong Xia, Mi Liu, Haijun Du, Zhiqiang Xia, Hailan Yao, Jun Han |
المصدر: | Viruses, Vol 15, Iss 5, p 1137 (2023) |
بيانات النشر: | MDPI AG, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Microbiology |
مصطلحات موضوعية: | CD147, anti-inflammation, T cell activation, Th cell subsets, viral myocarditis, Microbiology, QR1-502 |
الوصف: | Viral myocarditis (VMC) is a common disease characterized by cardiac inflammation. AC-73, an inhibitor of CD147, disrupts the dimerization of CD147, which participates in the regulation of inflammation. To explore whether AC-73 could alleviate cardiac inflammation induced by CVB3, mice were injected intraperitoneally with AC-73 on the fourth day post-infection (dpi) and sacrificed on the seventh dpi. Pathological changes in the myocardium, T cell activation or differentiation, and expression of cytokines were analyzed using H&E staining, flow cytometry, fluorescence staining and multiplex immunoassay. The results showed that AC-73 alleviated cardiac pathological injury and downregulated the percentage of CD45+CD3+ T cells in the CVB3-infected mice. The administration of AC-73 reduced the percentage of activated CD4+ and CD8+ T cells (CD69+ and/or CD38+) in the spleen, while the percentage of CD4+ T cell subsets in the spleen was not changed in the CVB3-infected mice. In addition, the infiltration of activated T cells (CD69+) and macrophages (F4/80+) in the myocardium also decreased after the AC-73 treatment. The results also showed that AC-73 inhibited the release of many cytokines and chemokines in the plasma of the CVB3-infected mice. In conclusion, AC-73 mitigated CVB3-induced myocarditis by inhibiting the activation of T cells and the recruitment of immune cells to the heart. Thus, CD147 may be a therapeutic target for virus-induced cardiac inflammation. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 15051137 1999-4915 |
العلاقة: | https://www.mdpi.com/1999-4915/15/5/1137Test; https://doaj.org/toc/1999-4915Test |
DOI: | 10.3390/v15051137 |
الوصول الحر: | https://doaj.org/article/8f8462887519438bb64b0043e459e478Test |
رقم الانضمام: | edsdoj.8f8462887519438bb64b0043e459e478 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 15051137 19994915 |
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DOI: | 10.3390/v15051137 |