Fig. 1
Preimmunization with αDCIR-PLP139–151 fusion antibodies (Abs) ameliorates EAE (PLP139–151 abbreviated in the figure as PLP due to space concerns). a Preimmunization with αDCIR2-PLP139–151 mAb (αDCIR2-PLP) ameliorates EAE in SJL/J mice. Pretreatment with the αDCIR2-PLP139–151 mAb prior to disease induction decreased severity of EAE in mice. Mice were injected i.p. with 1 μg of fusion antibodies (either αDCIR2-PLP139–151 mAb or ISO-PLP139–151 mAb (ISO-PLP) 10 days prior to disease induction (labeled as − 10), and EAE was induced starting on day 1. Mice were monitored daily for clinical signs of EAE, and disease severity was scored. Mean EAE scores for mice in each group (n = 5) are shown. Disease severity was decreased, and disease onset was delayed in mice that had been preimmunized with αDCIR2-PLP139–151 mAb. Mice that received αDCIR2-PLP139–151 mAb had significantly lower disease scores compared to controls that had not been pre-treated with any mAbs. Significant reduction of disease was observed on days 12 to 19 (p < 0.003) and days 22 to 30 (p < 0.009). Mice treated with DCIR2-PLP139–151 were also significantly different from control mice treated with ISO-PLP139–151 (p < 0.02 from days 12 to 17 and 24 to 28). The data presented represent three pooled independent experiments. b Using MPLA to induce maturation of DC concurrent with mAb administration abrogated the protective effect of preimmunization with DCIR2-PLP139–151. MPLA (10 μg) was co-administered with either αDCIR2-PLP139–151 mAb (n = 5) or ISO-PLP139–151 10 days before induction of EAE. To induce EAE, mice were injected with PLP139–151 in CFA. Pertussis toxin (PT) (200 ng) was administered into the tail vein the following day. Disease progression in mice that received MPLA with αDCIR2-PLP139–151 mAb was not significantly different from control mice treated with ISO/PLP139–151 mAb and MPLA (p > 0.05). c Adoptive transfer of splenocytes from mice treated with αDCIR2-PLP139–151. SJL/J mice were preimmunized i.p. with 1 μg of either αDCIR2-PLP139–151 mAb or αDCIR2 mAb alone ten days prior to induction of EAE. To induce disease, mice were immunized with 75 μg s.c. of PLP139–151 peptide, and 200 ng of pertussis toxin (pt) i.v. the next day. Splenocytes (5 × 106) were isolated from these animals 10 days after disease induction and injected intravenously into naïve SJL/J mice along with 75 μg s.c. of PLP139–151 in CFA, followed by PT (200 ng i.v.) the next day. Mice were monitored daily for clinical signs of EAE and disease severity was scored. Mean EAE scores mice in each group (n = 5) are shown. Mice that received splenocytes from animals that had been treated with αDCIR2-PLP139–151 mAb had significantly lower disease scores compared to recipients of spenocytes from control animals treated with αDCIR2 mAb alone. The difference in disease scores was observed days 15, 20–24 and 28 to 29 (p < 0.02, Student’s t-test). The experiment was repeated several times with similar results; a representative experiment is shown