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 3
Diminished CNS inflammation and axonal damage in MyD88- and TLR9-deficient mice. (A and B) Immunohistochemistry from WT and TLR2^–/–, TLR9^–/–, and MyD88^–/– mice. In all cases, animals with the highest clinical signs were taken either at peak of disease (day 20, A) or at the end of the experiment (day 35, B). Mac-3 staining in total spinal cord sections revealed similar strong macrophage infiltration in WT, TLR2^–/–, and TLR9^–/– mice at day 20 (A) whereas at later time points, TLR9^–/– mice revealed smaller infiltrates and MyD88^–/– mice revealed no infiltrates (B). Higher magnifications show CD3-positive lymphocytes, macrophages (Mac-3), regions of demyelination (luxol fast blue, LFB), and APP deposits representing axonal damage (APP). Scale bars: 500 μm (first column); 30 μm (second column).