Upregulated expression of Tim-3 involved in the process of toxoplasmic encephalitis in mouse model |
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Authors: | Bin Wu Bo Huang Ying Chen Shaoyuan Li Junping Yan Huanqin Zheng Shiguang Huang Jilong Shen Zhao-Rong Lun Yong Wang Lloyd H Kasper Fangli Lu |
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Institution: | 1. Department of Parasitology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China 2. Key Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou, 510080, Guangdong, China 3. Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China 4. Jinan University School of Medicine, Guangzhou, 510632, China 5. The Anhui Provincial Laboratory of Pathogen Biology, Anhui Medical University, Hefei, 230032, China 6. Center for Parasitic Organisms, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, China 7. Department of Pathogen Biology, Nanjing Medical University, Nanjing, 210029, China 8. Department of Microbiology/Immunology, Dartmouth Medical School, Lebanon, NH, USA
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Abstract: | Toxoplasma gondii can establish chronic infection and is characterized by the formation of tissue cysts in the brain. The cysts may remain throughout the life of the host but can reactivate and cause life-threatening toxoplasmic encephalitis (TE) in immunocompromised patients. T cell-mediated immune responses are essential for preventing the reactivation of chronic infection of T. gondii in the brain. The immunoinhibitory receptor T cell immunoglobulin and mucin domain (Tim)-1 and Tim-3 are expressed on terminally differentiated T helper (Th) 2 and Th1 cells, respectively, participating in the regulation of Th immune response. However, there is no report concerning the role of Tim genes in TE. In this study, Kunming outbred mice were infected with Prugniaud (Pru), a type II strain of T. gondii by oral gavage. Compared with the uninfected controls, there were mild brain inflammations at 3 weeks postinfection (p.i.), moderate brain inflammations at 5 weeks p.i., and aggravated brain inflammations and necrosis at 7 and 9 weeks p.i. The expressions of tachyzoite stage-specific genes in brains were consistent with the severity of brain histopathology of TE at 5 and 7 weeks p.i., while the expressions of bradyzoite stage-specific genes in brains were significantly increased at 7 and 9 weeks p.i. Using quantitative real-time PCR detection and immunohistochemistry staining, our results showed that the expressions of Tim-3 were significantly upregulated in both brains and spleens at 5 weeks p.i. and in spleens at 9 weeks p.i., which showed the similar dynamic tendency as that of interferon-γ expressions in both brains and spleens at the same times. In contrast, the Th2-specific marker Tim-1 expressions were significantly downregulated in both brains and spleens at 3 weeks p.i. and upregulated in both brains and spleens at 7 and 9 weeks p.i., which showed the similar dynamic tendency as that of interleukin-4 expressions in both brains and spleens at the same time. Our data indicate that Tim-3 may involve in the process of TE in mice infected with T. gondii Pru strain. |
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