Li Ye, Hui Chen, Chuanyi Ning, Ning Zang, Fangning Zhao, Jie Liu and Hao Liang
Guangxi Medical University, China
Posters & Accepted Abstracts: J AIDS Clin Res
Previous studies have shown the interaction between plasmacytoid dendritic cells (pDCs) and nature killer (NK) cells is critical for host innate immunity against viral infections. However, the pDC-NK interaction mechanisms as well as the effects of HIV/HCV infections on this interaction remain to be determined. According to the infection status, participants were enrolled and divided into four groups: HIV-1 monoinfection, HCV monoinfection, HIV/HCV co-infection and healthy control groups. pDCs and NK cells were isolated from PBMCs of the subjects and related cellular factors were measured and compared among different groups. From healthy subjects, the results showed that pDCs produced high level of IFN-�± through activation by TLR-9 receptor agonist ODN2216 treatment ex vivo; whereas NK cells were not directly activated by ODN2216 treatment but produced cytokines (IFN-�³, perforin, granzyme-B) by co-culture with ODN2216-activated pDCs. pDCs from viral infected patients (HIV, HCV, HIV/HCV) exhibited higher levels of IFN-�± compared to pDCs from healthy subjects, indicating viral infections could activiate pDCs in vivo. However, HIV infections (HIV, HIV/HCV) resulted in no response of pDC to ODN2216 treatment ex vivo, whereas HCV monoinfection had little effect on pDC activation by ODN2216 treatment. Correspondingly, in HIV and HIV/HCV groups, NK cells were no longer activated by co-culture with ODN2216-treated pDCs, whereas in HCV group, NK cells were still activated by co-culture with ODN2216-activated pDCs. Taken together, our results indicate that HIV infection impairs pDC function and thus disrupts subsequent pDC-NK interaction and HCV infection has little impact on pDC function and pDC-NK interaction.
Email: yeligx@163.com
Journal of AIDS & Clinical Research received 5264 citations as per Google Scholar report