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Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against an acute vaccinia infection in the lungs

Ning Yang, Joseph M. Luna, Peihong Dai, Yi Wang, Charles M. Rice, Liang Deng
doi: https://doi.org/10.1101/2020.01.20.910927
Ning Yang
1Dermatology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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  • For correspondence: dengl@mskcc.org yangn@mskcc.org
Joseph M. Luna
2The Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, United States
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Peihong Dai
1Dermatology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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Yi Wang
1Dermatology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
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Charles M. Rice
2The Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, United States
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Liang Deng
1Dermatology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
2The Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, United States
3Weill Cornell Medical College, New York, New York, USA
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  • For correspondence: dengl@mskcc.org yangn@mskcc.org
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SUMMARY

The pulmonary immune system consists of a network of tissue-resident cells as well as immune cells that are recruited to the lungs during infection and/or inflammation. How the two immune components cross-talk during an acute viral infection is not well understood. Intranasal infection of mice with vaccinia virus causes lethal pneumonia and systemic dissemination. Here we report that vaccinia host range protein C7 is a critical virulence factor. Vaccinia virus with deletion of C7 (VACVΔC7L) is non-pathogenic in wild-type C57BL/6J mice, but it gains virulence in mice lacking STAT2, or IFNAR1, or MDA5/STING. We provide evidence that lung type II alveolar epithelial cells (AECs) provide first-line of defense against VACVΔC7L infection by inducing IFN-β and IFN-stimulated genes via the activation of the MDA5 and STING-mediated nucleic acid-sensing pathways. This leads to recruitment of CCR2+ inflammatory monocytes into the lungs to fight against viral dissemination.

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Posted January 21, 2020.
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Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against an acute vaccinia infection in the lungs
Ning Yang, Joseph M. Luna, Peihong Dai, Yi Wang, Charles M. Rice, Liang Deng
bioRxiv 2020.01.20.910927; doi: https://doi.org/10.1101/2020.01.20.910927
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Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against an acute vaccinia infection in the lungs
Ning Yang, Joseph M. Luna, Peihong Dai, Yi Wang, Charles M. Rice, Liang Deng
bioRxiv 2020.01.20.910927; doi: https://doi.org/10.1101/2020.01.20.910927

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