| First Author | Shaabani N | Year | 2016 |
| Journal | Cell Death Dis | Volume | 7 |
| Issue | 11 | Pages | e2446 |
| PubMed ID | 27809306 | Mgi Jnum | J:357945 |
| Mgi Id | MGI:6844176 | Doi | 10.1038/cddis.2016.350 |
| Citation | Shaabani N, et al. (2016) CD169(+) macrophages regulate PD-L1 expression via type I interferon and thereby prevent severe immunopathology after LCMV infection. Cell Death Dis 7(11):e2446 |
| abstractText | 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. |
