Figure 5.

CD169⁺ macrophages prevent severe immunopathology during chronic viral infection. (a–c) Wild type (WT) and CD169 diphtheria toxin receptor (−DTR) mice were infected intravenously with 2 × 10⁴ plaque-forming units (PFU) of lymphocytic choriomeningitis virus strain Docile (LCMV-Docile) for 11 days. (a) Viral titers were measured in various organs (n=6). (b) Number of virus-specific Tet-GP33⁺ CD8⁺ T cells was determined in the spleen and liver (n=7–8). (c) IFN-γ⁺CD8⁺ T cells were counted in the spleen and liver (n=7–8). (d) WT and CD169-DTR mice were infected intravenously with 2 × 10⁴ PFU LCMV-Docile and treated with anti-CD8 depletion antibody or left untreated. Serum alanine aminotransferase (ALT) activity was measured after 13 days (n=3-4). (e) WT and CD169-DTR mice were infected intravenously with 2 × 10⁴ PFU LCMV-Docile and treated with anti-CD8 depletion antibody or left untreated. Survival of mice was monitored (n=8–33). (f and g) WT and programmed cell death protein 1-null (PD-1^–/–) mice were infected intravenously with 2 × 10⁴ PFU LCMV-Docile. (f) Serum ALT activity was measured after 13 days (n=3). (g) Survival of mice was monitored (n=3). NS, not significant, *P<0.05, ***P<0.001. Statistical significance was detected by Student's t-test (b, c, d and f) or log-rank (Mantel-Cox) test (e and g)