Fig. 3
From: NKG2A is a NK cell exhaustion checkpoint for HCV persistence
NKG2A blocking promoted HCV clearance. a C/OTg mice (n = 13) were infected with 1 mL HCV J399EM (TCID50 = 2 × 107/mL). b The self-limited infection in C/OTg mice exhibited an initial high peripheral viral load (<1 mpi) followed with RNA copies below the detection limit (≥1 mpi), whereas HCV persistent infection was characterized by sustained HCV viral loads in the serum beyond 1 mpi. c FACS analysis of NKG2A in peripheral NK cells and qPCR measurement of HCV RNA copies in the serum 1 m after C/OTg mice (n = 13) were infected. d C/OTg mice (n = 9 for each time point) were treated with anti-NKG2A or isotype Ig (100 μg/3 days, i.p.) 1 day before HCV infection. e qPCR measurement of HCV RNA copies in livers and sera; f FACS analysis of CD107a and granzyme B expression in NK cells; g FACS analysis of intracellular IFN-γ in isolated NK cells after co-cultured with Yac-1. h C/OTg mice (n = 6 for each time point) were treated with anti-NKG2A or isotype Ig (100 μg/3 days, i.p.) beginning at 2 wpi, i HCV RNA copies in livers and sera; j CD107a and granzyme B were measured in NK cells; and k HCV-specific CD8+ T cell response by IFN-γ ELISpot assays using splenocytes (4 × 105 for each well) isolated from mice 1 mpi. Epitope peptides (final concentration 4 μg/mL) were indicated. Dash lines indicated limits of detection (qPCR, 500 copies/mL serum or 100 copies/mg liver; ELISpot, 50 spots/4 × 105 splenocytes). Data were mean ± SD, Student t-test. *P < 0.05; **P < 0.01; ***P < 0.001. Source data are provided as a Source Data file
