SOCS1 restricts dendritic cells’ ability to break self tolerance and induce antitumor immunity by regulating IL-12 production and signaling
J. Clin. Invest. Kevin Evel-Kabler, et al. 116:90 doi:10.1172/JCI26169 [Go to this article.]

Figure 1
Persistent TLR stimulation of DC immunization failed to induce pathological autoimmune response and antitumor immunity. (A) TRP2-specific CTL responses induced by persistent in vivo TLR stimulation and DC immunization. C57BL/6 mice were immunized with TRP2-pulsed (100 μg/ml) and LPS-matured (100 ng/ml) DCs and then stimulated with various TLR agonists daily for 7 consecutive days. Splenocytes pooled from immunized mice (2–3 mice) were subjected to IFN-γ ELISPOT assays. An irrelevant peptide (OVA-I peptide) was used as a negative control. (B and C) Inability to control preestablished B16 tumors by persistent in vivo TLR stimulation and DC immunization. Groups of mice were inoculated s.c. with B16 tumor cells (2.5 × 10⁵) and 3 days later were immunized via the rear foot pad with 1.5 × 10⁶ TRP2 peptide–pulsed (100 μg/ml) DCs with ex vivo LPS maturation. After DC transfer, in vivo TLR agonists were administered i.p. daily for 7 days. Tumor growth and percent survival (n = 5–7 mice/group) curves represent 1 of 3 independent experiments. When their tumor volume reached approximately 2,000 mm³ in size, mice were euthanized and recorded as dead.