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. 2018 Apr 9;128(5):1971–1984. doi: 10.1172/JCI96791

Figure 2. OVA delivered by Clec9A-TNE promotes MyD88-dependent DC activation and IFN-α production.

Figure 2

(A) C57BL/6 mice were injected i.v. with OVA-Clec9A-TNE, OVA-isotype-TNE, Clec9A-TNE, or isotype-TNE. Six hours later, surface expression of CD86, CD80, and CD40 by CD8+ DCs, CD8– DCs, and pDCs was analyzed by flow cytometry (n = 6 from 2 separate experiments). (B) C57BL/6 or TLR4–/– mice were adoptively transferred with equal numbers of unpulsed CFSElo and SIINFEKL-pulsed CFSEhi target cells 6 days after i.v. injection with OVA-Clec9A-TNE or OVA-isotype-TNE. The percentage of SIINFEKL peptide–specific lysis in spleen is depicted (n = 7–12 from 3 separate experiments). (C and D) C57BL/6, Casp1–/–, IFNAR1–/–, MyD88–/–, or CD40–/– mice were injected i.v. with OVA-Clec9A-TNE. Six hours later the expression of CD86 by CD8+ splenic DCs was analyzed by flow cytometry (C) (n = 7 from 2 experiments), and IFN-α levels in serum from these mice were measured by ELISA (D). (E) C57BL/6 (WT), CASP1–/–, IFNAR1–/–, MyD88–/–, or CD40–/– mice were adoptively transferred with equal numbers of unpulsed CTVlo and SIINFEKL-pulsed CTVhi target cells 5 days after i.v. injection with OVA-Clec9A-TNE (n = 9–10 from 2 experiments). Specific killing of target cells is shown. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 by Tukey’s multiple-comparisons test.