Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 122, Issue 11, Pages 4037-4047Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI60659
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Funding
- NIH [U01 AI10008, R01 HL086899, R01AI046954, P01AI058113, U19AI083025, 1K99AI095320-01]
- Center for Research on Influenza Pathogenesis (CRIP), an National Institute of Allergy and Infectious Diseases Centers of Excellence for Influenza Research and Surveillance network [HHSN266200700010C]
- Fulbright-Generalitat de Catalunya
- Beatriu de Pinos postdoctoral fellowship
- [JDRF-17-2010-770]
- [DP2DK083052-01]
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CD8(+) cytotoxic T cells are critical for viral clearance from the lungs upon influenza virus infection. The contribution of antigen cross-presentation by DCs to the induction of anti-viral cytotoxic T cells remains controversial. Here, we used a recombinant influenza virus expressing a nonstructural 1-GFP (NS1-GFP) reporter gene to visualize the route of antigen presentation by lung DCs upon viral infection in mice. We found that lung CD103(+) DCs were the only subset of cells that carried intact GFP protein to the draining LNs. Strikingly, lung migratory CD103(+) DCs were not productively infected by influenza virus and thus were able to induce virus-specific CD8(+) T cells through the cross-presentation of antigens from virally infected cells. We also observed that CD103(+) DC resistance to infection correlates with an increased anti-viral state in these cells that is dependent on the expression of type I IFN receptor. These results show that efficient cross-priming by migratory lung DCs is coupled to the acquisition of an anti-viral status, which is dependent on the type I IFN signaling pathway.
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