A Protective Role for the Lectin CD169/Siglec-1 against a Pathogenic Murine Retrovirus.
Ontology highlight
ABSTRACT: 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
SUBMITTER: Uchil PD
PROVIDER: S-EPMC6331384 | biostudies-literature | 2019 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA