HIV controllers (HICs), rare HIV-1 infected individuals able to control viral replication without antiretroviral therapy, are characterized by an efficient polyfunctional and cytolytic HIV-specific CD8+ T cell response. The mechanisms underlying the induction and maintenance of such response in many HICs despite controlled viremia are not clear. Dendritic cells play a crucial role in the generation and reactivation of T cell responses but scarce information is available on those cells in HICs. We found that monocyte derived dendritic cells (MDDCs) from HICs are less permissive to HIV-1 infection than cells from healthy donors. In contrast MDDCs from HICs are particularly efficient at capturing HIV-1 particles when compared to cells from healthy donors or HIV-1 patients with suppressed viral load on antiretroviral treatment. MDDCs from HICs expressed on their surface high levels of syndecan-3, DC-SIGN and MMR, which could cooperate to facilitate HIV-1 capture. The combination of low susceptibility to HIV-1 infection but enhanced capacity to capture particles might allow MDDCs from HICs to preserve their function from the deleterious effect of infection while facilitating induction of HIV-specific CD8+ T cells by cross-presentation in a context of low viremia.
Dendritic Cells from HIV Controllers Have Low Susceptibility to HIV-1 Infection In Vitro but High Capacity to Capture HIV-1 Particles.
HIV 控制者体内的树突状细胞在体外对 HIV-1 感染的易感性较低,但捕获 HIV-1 颗粒的能力较强
阅读:8
作者:Hamimi Chiraz, David Annie, Versmisse Pierre, Weiss Laurence, Bruel Timothée, Zucman David, Appay Victor, Moris Arnaud, Ungeheuer Marie-Noëlle, Lascoux-Combe Caroline, Barré-Sinoussi Françoise, Muller-Trutwin Michaela, Boufassa Faroudy, Lambotte Olivier, Pancino Gianfranco, Sáez-Cirión Asier
| 期刊: | PLoS One | 影响因子: | 2.600 |
| 时间: | 2016 | 起止号: | 2016 Aug 9; 11(8):e0160251 |
| doi: | 10.1371/journal.pone.0160251 | 研究方向: | 细胞生物学 |
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
