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Contribution of IL-17 to mouse hepatitis virus strain 3-induced acute liver failure

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Summary

Recently, the Th17 cells and IL-17 have been shown to play a critical role in the immune-mediated liver injury in hepatitis B, while their functions in acute liver failure have not been well elucidated yet. In this study, we primarily investigated the role of IL-17 in the development of mouse hepatitis virus strain 3 (MHV-3)-induced acute liver failure. IL-17 mRNA levels in liver tissue were quantified by using quantitative real-time polymerase chain reaction, and cytokine IL-17 levels in liver tissue and serum were determined by using ELISA in MHV-3-induced murine fulminant hepatitis model. The IL-17 expression levels on CD4+T and CD8+T cells were determined by using flow cytometry. The correlation between IL-17 level and liver injury was studied. Th17 associated cytokines were also investigated by intracellular staining. Our results showed that the IL-17 expression was significantly elevated in the liver and serum of BALB/cJ mice infected with MHV-3. Moreover, a time course study showed that the percentage of both IL-17-producing CD4+T cells and IL-17-producing CD8+T cells was increased remarkably in the liver starting from 48 h and peaked at 72 h post-infection. There was a close correlation between hepatic or serum IL-17 concentration and the severity of liver injury defined by ALT level, respectively. Th17 associated cytokines, IL-6, IL-21 and IL-22, were also increased significantly at 72 h post-infection. It was concluded that IL-17 may contribute to the pathogenesis of MHV-3-induced acute liver failure.

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Correspondence to Qin Ning  (宁 琴).

Additional information

This project was supported by grants from National Science Foundation of China Advanced Program (No. 81030007), National Science Foundation of China for Young Scholar (No. 81100308/H0318).

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Zhu, L., Chen, T., Lu, Y. et al. Contribution of IL-17 to mouse hepatitis virus strain 3-induced acute liver failure. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 32, 552–556 (2012). https://doi.org/10.1007/s11596-012-0095-6

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  • DOI: https://doi.org/10.1007/s11596-012-0095-6

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