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. 2017 Mar 3;7:43315. doi: 10.1038/srep43315

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Copyright © 2017, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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(a) Left panel: Pro-inflammatory cytokines are at low levels in wild-type nerve (top), show increased protein levels in neurofibroma (middle), and are reduced after treatment of neurofibroma with PEGylated IFN-α2b (bottom). Right panel: Relative intensity, reflecting comparative levels of expression for each protein, after the intensity of pixels was averaged and plotted. (b) A model developed from gene expression analysis (drawn by Inkscape v0.48, http://inkscape.org). Decreased levels of type-I interferons and increased type-II interferon increase inflammation in the tumor microenvironment by increasing expression of Casp1 and Il1b mRNAs. CASP1 pro-protein is known to be cleaved and thus be activated by the inflammasome. Active CASP1 cleaves pro-IL1B protein, releasing active IL1B cytokine. (c) Based on this analysis, normal SCs suppress nerve inflammation. When Nf1^−/− SCs are present, de-regulated interferons result in inflammation, which can be largely normalized by PEGylated IFN-α2b.