期刊
BLOOD
卷 118, 期 19, 页码 5152-5162出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2011-03-344218
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资金
- Wellcome Trust [085164/Z/08/Z]
- National Institutes of Health [1R01MH087233-01A1, 2P01MH070306-06]
- Wellcome Trust [085164/Z/08/Z] Funding Source: Wellcome Trust
Adelicate balance between immunostimulatory and immunosuppressive signals mediated by dendritic cells (DCs) and other antigen-presenting cells (APCs) regulates the strength and efficacy of antiviral T-cell responses. HIV is a potent activator of plasmacytoid DCs (pDCs), and chronic pDC activation by HIV promotes the pathogenesis of AIDS. Cholesterol is pivotal in maintaining HIV envelope integrity and allowing HIV-cell interaction. By depleting envelope-associated cholesterol to different degrees, we generated virions with reduced ability to activate pDCs. We found that APC activation was dissociated from the induction of type I IFN-alpha/beta and indoleamine-2,3-dioxygenase (IDO)-mediated immunosuppression in vitro. Extensive cholesterol withdrawal, resulting in partial protein and RNA loss from the virions, rendered HIV a more powerful recall immunogen for stimulating memory CD8 T-cell responses in HIV-exposed, uninfected individuals. These enhanced responses were dependent on the inability of cholesterol-depleted HIV to induce IFN alpha/beta. (Blood. 2011;118(19):5152-5162)
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