Additional Supporting Information can be found in the online version of this article.

ANA_22511_sm_suppinfofig1.tif230KSupporting Information Figure 1. Clinical course, histopathology, and T cell proliferation in EAE TLR4-deficient mice. (A) Clinical course. Mice were immunized as indicated in Material and Methods. TLR4-deficient and wild-type mice developed clinical signs of EAE and displayed the same chronic non-remitting clinical course. Data are expressed as mean (standard error of the mean). (B) Histopathology. Spinal cord cross sections stained with hematoxylin and eosin (left panels) and Kluver-Barrera (right panels) of wild-type (upper panels) and TLR4-deficient (lower panels) EAE mice. No differences were observed in the inflammatory infiltration (left panels) and demyelination (right panels) between groups. (C) T cell proliferation. Spleen cells were obtained from mice at day 14 post-immunization and stimulated with MOG35-55, LPS or PHA. For the proliferation assay, cells were pulse-labeled with [3H]thymidine, and radioactivity was measured. Bars indicate mean values (standard deviation) of stimulation index (n=4). Stimulation index is expressed as mean of counts per minute (cpm) from MOG35-55, PHA or LPS cultures divided by cpm mean of non-stimulated cultures (for MOG35-55, p=0.486; for LPS p=0.114; for PHA p=0.700; Mann-Whitney's test). MOG: myelin oligodendrocyte glycoprotein. LPS: lipopolysaccharide. PHA: phytohemagglutinin.
ANA_22511_sm_suppinfotab1.doc34KSupporting Table 1. Sequence of primers used for real-time PCR absolute quantification
ANA_22511_sm_suppinfo.doc26KSupporting Information

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