Innate immunity mediated by TLR9 modulates pathogenicity in an animal model of multiple sclerosis
J. Clin. Invest. Marco Prinz, et al. 116:456 doi:10.1172/JCI26078 [Go to this article.]

Figure 4
Nonhematopoietic TLR signaling is involved in EAE disease. (A–C) Active EAE in MyD88 (A and B) and TLR9 (C) BM chimeric mice. After BM reconstitution, mice were allowed to recover for 6–8 weeks, then immunized with MOG_35–55 in CFA as described and scored for disease (means). Statistically significant data points are marked with asterisks. P < 0.05. Results are representative of 2 independent experiments. (B) Quantification of mononuclear infiltrates and axonal damage in MyD88 chimeric mice. For each genotype, at least 4 diseased spinal cords were used for quantification (means ± SD). Arrows indicate direction of bone marrow reconstitution.