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Full-Text Articles in Internal Medicine
Hcv-Associated Exosomes Promote Myeloid-Derived Suppressor Cell Expansion Via Inhibiting Mir-124 To Regulate T Follicular Cell Differentiation And Function, Ling Wang, Dechao Cao, Ling Wang, Juan Zhao, Lam Nhat Nguyen, Xindi Dang, Yingjie Ji, Xiao Y. Wu, Zheng D. Morrison, Qian Xie, Mohamed El Gazzar, Shunbin Ning, Jonathon P. Moorman, Zhi Q. Yao
Hcv-Associated Exosomes Promote Myeloid-Derived Suppressor Cell Expansion Via Inhibiting Mir-124 To Regulate T Follicular Cell Differentiation And Function, Ling Wang, Dechao Cao, Ling Wang, Juan Zhao, Lam Nhat Nguyen, Xindi Dang, Yingjie Ji, Xiao Y. Wu, Zheng D. Morrison, Qian Xie, Mohamed El Gazzar, Shunbin Ning, Jonathon P. Moorman, Zhi Q. Yao
ETSU Faculty Works
Virus-infected cells can regulate non-permissive bystander cells, but the precise mechanisms remain incompletely understood. Here we report that this process can be mediated by transfer of viral RNA-loaded exosomes shed from infected cells to myeloid-derived suppressor cells (MDSCs), which in turn regulate the differentiation and function of T cells during viral infection. Specifically, we demonstrated that patients with chronic hepatitis C virus (HCV) infection exhibited significant increases in T follicular regulatory (TFR) cells and decreases in T follicular helper (TFH) cells. These MDSC-mediated T-cell dysregulations resulted in an increased ratio of TFR/TFH and IL-10 production in peripheral blood. Specifically, co-culture …
Inhibition Of Trf2 Accelerates Telomere Attrition And Dna Damage In Naïve Cd4 T Cells During Hcv Infection, Lam Nhat Nguyen, Juan Zhao, Dechao Cao, Xindi Dang, Ling Wang, Jianqi Lian, Ying Zhang, Zhansheng Jia, Xiao Y. Wu, Zheng Morrison, Qian Xie, Yingjie Ji, Zheng Zhang, Mohammed El Gazzar, Shunbin Ning, Jonathan P. Moorman, Zhi Q. Yao
Inhibition Of Trf2 Accelerates Telomere Attrition And Dna Damage In Naïve Cd4 T Cells During Hcv Infection, Lam Nhat Nguyen, Juan Zhao, Dechao Cao, Xindi Dang, Ling Wang, Jianqi Lian, Ying Zhang, Zhansheng Jia, Xiao Y. Wu, Zheng Morrison, Qian Xie, Yingjie Ji, Zheng Zhang, Mohammed El Gazzar, Shunbin Ning, Jonathan P. Moorman, Zhi Q. Yao
ETSU Faculty Works
T cells play a crucial role in viral clearance and vaccine responses; however, the mechanisms that regulate their homeostasis during viral infections remain unclear. In this study, we investigated the machineries of T-cell homeostasis and telomeric DNA damage using a human model of hepatitis C virus (HCV) infection. We found that naïve CD4 T cells in chronically HCV-infected patients (HCV T cells) were significantly reduced due to apoptosis compared with age-matched healthy subjects (HSs). These HCV T cells were not only senescent, as demonstrated by overexpression of aging markers and particularly shortened telomeres; but also DNA damaged, as evidenced by …
Insufficiency Of Dna Repair Enzyme Atm Promotes Naive Cd4 T-Cell Loss In Chronic Hepatitis C Virus Infection, Juan Zhao, Xindi Dang, Peixin Zhang, Lam Nhat Nguyen, Dechao Cao, Lin Wang, Xiaoyuan Wu, Zheng D. Morrison, Ying Zhang, Zhansheng Jia, Qian Xie, Ling Wang, Shunbin Ning, Mohamed El Gazzar, Jonathan P. Moorman, Zhi Q. Yao
Insufficiency Of Dna Repair Enzyme Atm Promotes Naive Cd4 T-Cell Loss In Chronic Hepatitis C Virus Infection, Juan Zhao, Xindi Dang, Peixin Zhang, Lam Nhat Nguyen, Dechao Cao, Lin Wang, Xiaoyuan Wu, Zheng D. Morrison, Ying Zhang, Zhansheng Jia, Qian Xie, Ling Wang, Shunbin Ning, Mohamed El Gazzar, Jonathan P. Moorman, Zhi Q. Yao
ETSU Faculty Works
T cells have a crucial role in viral clearance and vaccine response; however, the mechanisms regulating their responses to viral infections or vaccinations remain elusive. In this study, we investigated T-cell homeostasis, apoptosis, DNA damage, and repair machineries in a large cohort of subjects with hepatitis C virus (HCV) infection. We found that naive CD4 T cells in chronically HCV-infected individuals (HCV T cells) were significantly reduced compared with age-matched healthy subjects. In addition, HCV T cells were prone to apoptosis and DNA damage, as evidenced by increased 8-oxoguanine expression and γH2AX/53BP1-formed DNA damage foci—hallmarks of DNA damage responses. Mechanistically, …