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. 2015 Jun 17;195(3):841–852. doi: 10.4049/jimmunol.1403063

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Copyright © 2015 by The American Association of Immunologists, Inc.

This article is distributed under The American Association of Immunologists, Inc., Reuse Terms and Conditions for Author Choice articles.

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FIGURE 8. — Overproduction of NO and axonal damage in atypical EAE. (A) CRB-, BS-, and SC-infiltrating mononuclear cells isolated at the peak of disease from SOCS3^fl/fl mice with classical EAE or LysMCre-SOCS3^fl/fl mice with atypical EAE were cultured for 24 h, and supernatants were analyzed for nitrite by the Griess reaction (n = 4 cultures/group). Mean ± SD. (B) Protein extracts from CRB of unimmunized (UN) or MOG_35–55-immunized SOCS3^fl/fl with classical EAE or LysMCre-SOCS3^fl/fl mice with atypical EAE were immunoblotted with the indicated Abs. **p < 0.01.