In:
Cell Death & Disease, Springer Science and Business Media LLC, Vol. 7, No. 11 ( 2016-11-03), p. e2446-e2446
Abstract:
Upon infection with persistence-prone virus, type I interferon (IFN-I) mediates antiviral activity and also upregulates the expression of programmed death ligand 1 (PD-L1), and this upregulation can lead to CD8 + T-cell exhaustion. How these very diverse functions are regulated remains unknown. This study, using the lymphocytic choriomeningitis virus, showed that a subset of CD169 + macrophages in murine spleen and lymph nodes produced high amounts of IFN-I upon infection. Absence of CD169 + macrophages led to insufficient production of IFN-I, lower antiviral activity and persistence of virus. Lack of CD169 + macrophages also limited the IFN-I-dependent expression of PD-L1. Enhanced viral replication in the absence of PD-L1 led to persistence of virus and prevented CD8 + T-cell exhaustion. As a consequence, mice exhibited severe immunopathology and died quickly after infection. Therefore, CD169 + macrophages are important contributors to the IFN-I response and thereby influence antiviral activity, CD8 + T-cell exhaustion and immunopathology.
Type of Medium:
Online Resource
ISSN:
2041-4889
DOI:
10.1038/cddis.2016.350
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2016
detail.hit.zdb_id:
2541626-1
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