Exogenous IFNα can overcome the absence of DC-derived IL-12 in the induction of autoimmunity.

<p>(A) IFNα production was measured in the supernatant from unstimulated, LPS stimulated and PolyI∶C stimulated p40+/+ and p40−/− BMDCs by ELISA. Results are from 4 mice per treatment group and representative of 3 independent experiments. (B) Diabetes incidence in RIP-gp mice treated with IFNα alone (open diamond), peptide-pulsed p40−/− BMDCs stimulated with LPS (open square) or peptide-pulsed p40−/− BMDCs stimulated with LPS plus IFNα (open triangle). Injection of 10000 u of IFNα to RIP-gp mice 3 days after treatment with LPS stimulated peptide-pulsed 40−/− BMDCs or LPS and IFNα stimulated peptide-pulsed p40−/− BMDCs (open circle and open upside-down triangle respectively). (C) Diabetes incidence in IFNαR+/+/RIP-gp bone marrow chimeras treated with LPS stimulated p40+/+ BMDCs (open circle) and IFNαR−/−/RIP-gp chimeras treated with LPS stimulated p40−/− BMDCs (open square) or an additional i.v. injection of IFNα 3 days later (open triangle). A test of statistical significance of p<0.05 against RIP-gp mice (B) and IFNαR−/−/RIP-gp mice (C) treated with p40−/− BMDCs stimulated with LPS is denoted with *. Results shown are from a minimum of 6 mice per group from 2 independent experiments.