Induction of EAE in Ido1 deficient mice appeared to exacerbate pathology compared to C57BL/6 mice, indicated by a slight increase in the percentage of spinal cord demyelination, but this effect did not reach statistical significance ( Fig. 4 D). 4 Discussion The current experiments were designed to test the role of Ido1 and Ido2 during the pathogenesis of EAE.
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Deletion of indoleamine 2,3 dioxygenase (Ido)1 but not Ido2 exacerbates disease symptoms of MOG<sub>35-55</sub>-induced experimental autoimmune encephalomyelitis.
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Our data show that Ido1 −/− mice exhibit exacerbated clinical symptoms of EAE, characterized by greater weight loss during peak disease, an increase in maximal clinical score and a strong trend towards increased spinal cord pathology compared to C57BL/6 or Ido2 −/− mice.