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TLR-9 Activation Aggravates Concanavalin A-Induced Hepatitis via Promoting Accumulation and Activation of Liver CD4⁺ NKT Cells¹

Institute of Immunology, Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, China

Increasing evidence suggests that TLRs are involved in the pathogenesis of liver diseases; however, the underlying mechanisms remain obscure. In this study, we found that treatment with CpG-oligodeoxynucleotide (ODN) promoted the accumulation and activation of murine hepatic NKT cells. Additional experiments showed that CpG-ODN preferred to act on CD4⁺ NKT cells, while having less effect on CD4^– NKT cells. The effect of CpG-ODN on liver NKT cells depended on the presence of Kupffer cells and IL-12. Meanwhile, CpG-ODN pretreatment aggravated liver injury and promoted the production of inflammatory cytokines in a Con A-induced fulminant hepatitis model via TLR9 activation. Collectively, our data demonstrate that TLR9 stimulation prefers to promote the accumulation and activation of hepatic CD4⁺ NKT cells and suggest that TLR9 signaling might be involved in the pathogenesis of human hepatitis.

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¹ This work was supported by Natural Science Foundation of China Grants 30630059, 30721002, and 30730084 and Ministry of Science and Technology of China 973 Basic Science Project Grants 2007CB512405, 2007CB512807, 2007CB815800, and 2009CB522403.

² Address correspondence and reprint requests to Dr. Rui Sun or Dr. Zhigang Tian, School of Life Sciences, University of Science and Technology of China, 443 Huang-shan Road, Hefei 230027, China. E-mail addresses: sunr{at}ustc.edu.cn and tzg{at}ustc.edu.cn

³ Abbreviations used in this paper: ODN, oligodeoxynucleotide; ALT, alanine aminotransferase; DC, dendritic cell; DN, double negative; FasL, Fas ligand; MNC, mononuclear cell.

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