机构地区:[1]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences&Yunnan Province,Kunming Institute of Zoology,Chinese Academy of Sciences,Kunming,China [2]Graduate University of the Chinese Academy of Sciences,Beijing,China [3]CAS Key Laboratory of Infection and Immunity,Institute of Biophysics,Chinese Academy of Sciences,Beijing,China
出 处:《Cellular & Molecular Immunology》2012年第5期410-416,共7页中国免疫学杂志(英文版)
基 金:ACKNOWLEDGEMENTS This work was supported in part by grants from the National Basic Research Program of China (2009CB522306 and 2012CBA01305), the National Natural Science Foundation of China (30872317, 30800113, U0832601 and 81172876), the Knowledge Innovation Program of CAS (KSCX1-YW-10 and KSCX2-EW-R-13), the Key Scientific and Technological Program of China (2009ZX09501-029, 2012ZX10001-006 and 2012ZX10001-007) and Yunnan province (2010GA001) and the 'Western Light' Projects of the CAS. The funding organizations had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
摘 要:It is currently widely accepted that immune activation in HIV-infected individuals leads to a severe loss of CD4+ T cells and the progression to AIDS. However, the underlying mechanism of this immune activation remains unclear. Experimental data suggest that the activation of plasmacytoid dendritic cells (pDCs) by plasma viremia may play a critical role in HIV-induced immune activation. In this study, we found that the level of immune activation was higher in the late phase of SIVmac239 infection compared with chronic infection, which suggests that immune activation might be related to disease progression in SIVmac239-infected non-human primate models. Our work also showed that chloroquine could effectively inhibit the activation of pDCs in vitro and in vivo. However, chloroquine treatment of SIVmac239-infected macaques had no significant influence on the Cellular composition of peripheral blood in these animals.It is currently widely accepted that immune activation in HIV-infected individuals leads to a severe loss of CD4+ T cells and the progression to AIDS. However, the underlying mechanism of this immune activation remains unclear. Experimental data suggest that the activation of plasmacytoid dendritic cells (pDCs) by plasma viremia may play a critical role in HIV-induced immune activation. In this study, we found that the level of immune activation was higher in the late phase of SIVmac239 infection compared with chronic infection, which suggests that immune activation might be related to disease progression in SIVmac239-infected non-human primate models. Our work also showed that chloroquine could effectively inhibit the activation of pDCs in vitro and in vivo. However, chloroquine treatment of SIVmac239-infected macaques had no significant influence on the Cellular composition of peripheral blood in these animals.
关 键 词:Chinese rhesus macaque CHLOROQUINE immune activation pDC SIV
分 类 号:S858.31[农业科学—临床兽医学] N031[农业科学—兽医学]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...