Journal
SCIENCE IMMUNOLOGY
Volume 2, Issue 13, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aai8071
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Categories
Funding
- Ministere de l'Education Nationale de la Recherche et de Technologie fellowship
- Sidaction
- ATIP-Avenir program
- Ville de Paris Emergence program
- European FP7 Marie Curie Actions
- Labex VRI [ANR-10-LABX-77]
- Labex DCBIOL [ANR-10-IDEX-0001-02 PSL*, ANR-11-LABX-0043]
- ACTERIA Foundation
- Fondation Schlumberger pour l'Education et la Recherche (FSER)
- European Research Council [309848 HIVINNATE]
- ANRS (France REcherche Nord AMP
- Sud Sida-hiv Hepatites)
- Baylor Research Institute (BRI)
- NIH [U19AI057234, U19AI089987, R01DA033773, 1U19 AI 118610-01, U19AI117873, UO1AI095611]
- Center for Research on Influenza Pathogenesis [NIAID CEIRS HHSN272201400008C]
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Dendritic cells (DCs) are critical for the launching of protective T cell immunity in response to viral infection. Viruses can directly infect DCs, thereby compromising their viability and suppressing their ability to activate immune responses. How DC function is maintained in light of this paradox is not understood. By analyzing the susceptibility of primary human DC subsets to viral infections, we report that CD141(+) DCs have an innate resistance to infection by a broad range of enveloped viruses, including HIV and influenza virus. In contrast, CD1c(+) DCs are susceptible to infection, which enables viral antigen production but impairs their immune functions and survival. The ability of CD141(+) DCs to resist infection is conferred by RAB15, a vesicle-trafficking protein constitutively expressed in this DC subset. We show that CD141(+) DCs rely on viral antigens produced in bystander cells to launch cross-presentation-driven T cell responses. By dissociating viral infection from antigen presentation, this mechanism protects the functional capacity of DCs to launch adaptive immunity against viral infection.
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