期刊
SCIENCE IMMUNOLOGY
卷 6, 期 65, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.abi9331
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资金
- Francis Crick Institute from Cancer Research UK [FC001136, FC001206, FC001144]
- Francis Crick Institute from UK Medical Research Council [FC001136, FC001206, FC001144]
- Francis Crick Institute from Wellcome Trust [FC001136, FC001206, FC001144]
- ERC Advanced Investigator Grants [AdG 268670, 786674, 787826]
- Wellcome Investigator Award [WT106973MA]
- Boehringer Ingelheim Fonds
- EMBO Fellowship [ALTF 1096-2018]
- Marie Curie Fellowship [837951]
- Wellcome Trust [FC001136, FC001206, FC001144, WT106973MA]
- Marie Curie Actions (MSCA) [837951] Funding Source: Marie Curie Actions (MSCA)
- European Research Council (ERC) [786674, 787826] Funding Source: European Research Council (ERC)
Protection from respiratory viruses like influenza A virus (IAV) requires T cell-mediated immune responses initiated by conventional dendritic cells (cDCs) in the respiratory tract. Reinforcing the resident lung cDC network by cDC progenitors is necessary for effective induction of T cell responses against IAV in mice. Chemokines produced during IAV infection recruit pre-cDCs from blood, directing them to infection sites to increase cDC numbers and amplify T cell responses.
Protection from infection with respiratory viruses such as influenza A virus (IAV) requires T cell-mediated immune responses initiated by conventional dendritic cells (cDCs) that reside in the respiratory tract. Here, we show that effective induction of T cell responses against IAV in mice requires reinforcement of the resident lung cDC network by cDC progenitors. We found that CCR2-binding chemokines produced during IAV infection recruit pre-cDCs from blood and direct them to foci of infection, increasing the number of progeny cDCs next to sites of viral replication. Ablation of CCR2 in the cDC lineage prevented this increase and resulted in a deficit in IAV-specific T cell responses and diminished resistance to reinfection. These data suggest that the homeostatic network of cDCs in tissues is insufficient for immunity and reveal a chemokine-driven mechanism of expansion of lung cDC numbers that amplifies T cell responses against respiratory viruses.
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