Fig. 2: vCD44BP attenuates viral clearance by interfering with CD8 T cell functions.
From: Fibroblastic reticular cells direct the initiation of T cell responses via CD44
a, Viral loads in spleens of BALB/c mice infected with wild-type (MCMV), ∆vCD44BP or ∆CD44BP-REV (REV) MCMV viruses (MCMV: 2 dpi, n = 11; 4 dpi, n = 14; 6 dpi, n = 13; 10 dpi, n = 13; ∆vCD44BP: 2 dpi n = 11; 4 dpi, n = 14; 6 dpi, n = 15; 10 dpi, n = 20; REV: 2 dpi, n = 12; 4 dpi, n = 8; 6 dpi, n = 10; 10 dpi, n = 10). PFU, plaque-forming units. b, Viral loads in spleens of BALB/c mice depleted of CD4 (with GK1.5) or CD8 (with 53.5.8) T cells and infected with REV or ∆vCD44BP (4 dpi: REV, anti-CD4 and anti-CD8, n = 9; undepleted (−), n = 8; 6 dpi: REV, n = 8; undepleted and anti-CD4, n = 9; anti-CD8, n = 10). c, Viral loads in spleens of BALB/c (wild-type (WT)) and BALB/c Ifng−/− mice infected with MCMV or ∆vCD44BP (6 dpi: MCMV in WT, n = 12; ∆vCD44BP in WT, n = 11; MCMV in Ifng−/−, n = 17; ∆vCD44BP in Ifng−/−, n = 11; 10 dpi: MCMV in WT, n = 9; ∆vCD44BP in WT, n = 10; MCMV in Ifng−/−, n = 7; ∆vCD44BP in Ifng−/−, n = 13). Data in a–c are pooled from at least three independent experiments. d, Viral loads at 6 dpi in spleens of BALB/c wild-type and Pfp−/− mice infected with MCMV or ∆vCD44BP; pooled from two independent experiments (MCMV in WT n = 4; ∆vCD44BP in WT, n = 5; MCMV in Pfp−/− and ∆vCD44BP in Pfp−/−, n = 11). Mice were infected with 1 × 104 PFU, except in d, where 2 × 103 PFU was used. Graphs show mean ± s.e.m.; significance tested by two-sided Mann–Whitney test, or Kruskal–Wallis (in b only).
