作者: Corine H. GeurtsvanKessel , Monique A.M. Willart , Leonie S. van Rijt , Femke Muskens , Mirjam Kool
DOI: 10.1084/JEM.20071365
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摘要: Although dendritic cells (DCs) play an important role in mediating protection against influenza virus, the precise of lung DC subsets, such as CD11b− and CD11b+ conventional DCs or plasmacytoid (pDCs), different compartments is currently unknown. Early after intranasal infection, tracheal CD11b−CD11chi migrated to mediastinal lymph nodes (MLNs), acquiring co-stimulatory molecules process. This emigration from was followed by accumulation CD11b+CD11chi trachea interstitium. In MLNs, contained abundant viral nucleoprotein (NP), but these failed present antigen CD4 CD8 T cells, whereas resident CD11b−CD8α+ presented migratory CD11b−CD8α− cells. When CD11chi macrophages langerin+CD11b−CD11chi were depleted using either CD11c–diphtheria toxin receptor (DTR) langerin-DTR mice, development virus-specific CD8+ severely delayed, which correlated with increased clinical severity a delayed clearance. 120G8+ CD11cint pDCs also accumulated LNs carrying NP, their absence, there no effect on clearance severity. Rather, pDC-depleted reduction antiviral antibody production virus. suggests that multiple are endowed tasks