Journal
CELL REPORTS
Volume 29, Issue 10, Pages 3047-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.10.118
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Funding
- National Institute of Allergy and Infectious Diseases (NIAID) [R0AI110457, R01AI065544]
- National Institute on Aging (NIA) [R01AG048602, F32AI129352]
- National Cancer Institute of the National Institutes of Health (NIH) [P30CA056036]
- Thomas Jefferson University + Philadelphia University Open Access Fund
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During disseminating viral infections, a swift innate immune response (IIR) in the draining lymph node (dLN) that restricts systemic viral spread is critical for optimal resistance to disease. However, it is unclear how this IIR is orchestrated. We show that after footpad infection of mice with ectromelia virus, dendritic cells (DCs) highly expressing major histocompatibility complex class II (MHC class IIhi DCs), including CD207(+) epidermal Langerhans cells (LCs), CD103(+)CD207(+) double-positive dermal DCs (DP-DCs), and CD103(-)CD207(-) double-negative dermal DCs (DN-DCs) migrate to the dLN from the skin carrying virus. MHC class IIhi DCs, predominantly LCs and DP-DCs, are the first cells upregulating IIR cytokines in the dLN. Preventing MHC class IIhi DC migration or depletion of LCs, but not DP-DC deficiency, suppresses the IIR in the dLN and results in high viral lethality. Therefore, LCs are the architects of an early IIR in the dLN that is critical for optimal resistance to a disseminating viral infection.
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