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. Author manuscript; available in PMC: 2021 Aug 1.
Published in final edited form as: Nat Neurosci. 2021 Feb 1;24(2):234–244. doi: 10.1038/s41593-020-00770-9

Figure 6: Interferon gamma signaling regulates scar formation following neuroinflammation.

Figure 6:

a. Spinal cord sections from fibrotic cell-specific IFNγ knockout mice (fIFNγ, IFNγfl/fl; Col1a2CreERT) and littermate controls (IFNγfl/fl) stained for Col1 (green), CD11b (red) or CD31 (red), and DAPI (blue). The amount of fibrotic scar covering the lesion was quantified in (b), ± s.e.m., **p = 0.0039 by Student’s two-tailed t-test, n=14 control, 15 fIFNγ. c. EAE score for the fIFNγ mice and controls up to 30 days post EAE induction (± s.e.m., n= 14 control, 15 fIFNγ). d. Quantification of the CD11b+ immune cell area in the control and fIFNγ groups 30 days post EAE immunization, ± s.e.m., p = 0.61 by Student’s two-tailed t-test, n= 14 control, 15 fIFNγ. e. Quantification of the percentage of the total white matter area that is FluoroMyelin positive for the control and fIFNγ groups, ± s.e.m., p = 0.44 by Student’s two-tailed t-test, n= 14 control, 15 fIFNγ. f. Quantification of OLIG2+ cells per CD11b+ lesion area between the control and fIFNγ groups, ± s.e.m., p = 0.76 by Student’s two-tailed t-test, n= 14 control, 15 fIFNγ.