Figure 4. Normal IFN response to poly(I:C) and viruses in TLR3-mutated PBMCs. (A) PBMCs from four CTLs, P3, P3’s parents, and a TLR3−/− patient were infected with various types of viruses: double-stranded DNA (dsDNA; HSV-1) and single-stranded RNA (ssRNA−; IAV strain pH1N1, VSV, Sendai virus, mumps virus, measles virus, HPIV3) viruses. The levels of IFN-α, -β, and -λ and IL-6 were measured by ELISA 24 h after infection. (B) The induction of IFNL1, IFNB, MX1, OAS1, and ISG15 mRNA was assessed by RT-qPCR in PBMCs from four CTLs, P3, P3’s parents, and a TLR3−/− patient. RNA was isolated from these cells after 8 h of poly(I:C) stimulation and 24 h of IAV pH1N1 and HSV-1 infection. Mean values ± SD were calculated from biological duplicates from two independent experiments.
Figure 4.

Normal IFN response to poly(I:C) and viruses in TLR3-mutated PBMCs. (A) PBMCs from four CTLs, P3, P3’s parents, and a TLR3−/− patient were infected with various types of viruses: double-stranded DNA (dsDNA; HSV-1) and single-stranded RNA (ssRNA−; IAV strain pH1N1, VSV, Sendai virus, mumps virus, measles virus, HPIV3) viruses. The levels of IFN-α, -β, and -λ and IL-6 were measured by ELISA 24 h after infection. (B) The induction of IFNL1, IFNB, MX1, OAS1, and ISG15 mRNA was assessed by RT-qPCR in PBMCs from four CTLs, P3, P3’s parents, and a TLR3−/− patient. RNA was isolated from these cells after 8 h of poly(I:C) stimulation and 24 h of IAV pH1N1 and HSV-1 infection. Mean values ± SD were calculated from biological duplicates from two independent experiments.

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