Figure 4
Disruption of ITAM signaling is protective in EAE and inhibits autoreactive T-cell priming. (A) Mice were immunized with MOG35-55 peptide and pertussis toxin to induce disease. During the course of disease, mice were assigned a clinical score with grade 1, tail weakness; grade 2, hind limb weakness sufficient to impair righting; grade 3, one limb plegic; grade 4, hind limb paralysis; grade 5, moribund. Data are expressed as mean clinical score ± SD for n ≥ 5 mice per group. After the peak of disease (3 weeks), spinal chords were harvested and stained with hematoxylin and eosin (B). In addition, spleens were recovered and restimulated in vitro with MOG peptide to determine autoreactive T-cell frequencies by ELISPOT (C) and proliferation by thymidine incorporation (D). Data represent the mean ± SD for n ≥ 5 mice per group; *P < .05.

Disruption of ITAM signaling is protective in EAE and inhibits autoreactive T-cell priming. (A) Mice were immunized with MOG35-55 peptide and pertussis toxin to induce disease. During the course of disease, mice were assigned a clinical score with grade 1, tail weakness; grade 2, hind limb weakness sufficient to impair righting; grade 3, one limb plegic; grade 4, hind limb paralysis; grade 5, moribund. Data are expressed as mean clinical score ± SD for n ≥ 5 mice per group. After the peak of disease (3 weeks), spinal chords were harvested and stained with hematoxylin and eosin (B). In addition, spleens were recovered and restimulated in vitro with MOG peptide to determine autoreactive T-cell frequencies by ELISPOT (C) and proliferation by thymidine incorporation (D). Data represent the mean ± SD for n ≥ 5 mice per group; *P < .05.

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