期刊
CELL HOST & MICROBE
卷 25, 期 1, 页码 87-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2018.11.011
关键词
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资金
- NIH [R01 CA098727, P50GM082545]
- Flow Cytometry Shared Resource of the Yale Cancer Center [P30 CA016359]
- Yale Center for Cellular and Molecular Imaging [S10 OD020142, R21 AI112418]
- Francis Crick Institute [FC001099]
- China Scholarship Council
Lymph- and blood-borne retroviruses exploit CD169/Siglec-1-mediated capture by subcapsular sinus and marginal zone metallophilic macrophages for trans-infection of permissive lymphocytes. However, the impact of CD169-mediated virus capture on retrovirus dissemination and pathogenesis in vivo is unknown. In a murine model of the splenomegaly-inducing retrovirus Friend virus complex (FVC) infection, we find that while CD169 promoted draining lymph node infection, it limited systemic spread to the spleen. At the spleen, CD169-expressing macrophages captured incoming blood-borne retroviruses and limited their spread to the erythroblasts in the red pulp where FVC manifests its pathogenesis. CD169-mediated retroviral capture activated conventional dendritic cells 1 (cDC1s) and promoted cytotoxic CDS(+)8 cell responses, resulting in efficient clearing of FVC-infected cells. Accordingly, CD169 blockade led to higher viral loads and accelerated death in susceptible mouse strains. Thus, CD169 plays a protective role during FVC pathogenesis by reducing viral dissemination to erythroblasts and eliciting an effective cytotoxic T lymphocyte response via cDC1s.
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