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Figure 2 | Journal of Neuroinflammation

Figure 2

From: IFN-gamma signaling in the central nervous system controls the course of experimental autoimmune encephalomyelitis independently of the localization and composition of inflammatory foci

Figure 2

Peripheral immune responses and CNS leukocyte accumulation are not correlated with the incidence of atypical symptoms. Cell subsets isolated from Percoll-fractionated CNS (pooled spinal cord and brain) showing significant changes by flow cytometry between the various groups of mice with EAE. Neutrophils (A) and Th17 cells (C) were significantly upregulated on days 14 and 21 pi, and total CD4+ T cells on day 14 (B) in the CNS of IFNγ-/- compared to WT controls. The CNS of IFNγRKO-chimeras and IFNγRperiKO mice, on day 21 (but not day 14) pi was populated by greater numbers of neutrophils (Ly6G+GR1+) compared to WT-chimeras and IFNγRCNSKO mice (D). Infiltrating macrophages were significantly upregulated only in the CNS of WT-chimeras (CD11b+CD45.1hiLy6G-) and IFNγRperiKO mice (CD11b+CD45.2hiLy6G-) both on day 14 and 21 pi (E). Fewer Th17 cells were detected in the CNS of IFNγRperiKO mice compared to the other groups only on day 14 pi (F). Data are presented as means ± SEMs, n = 6-9; significance was calculated using the Mann-Whitney test with Bonferroni correction for the WT and IFNγ-/- groups and with the non-parametric Kruskal-Wallis with post-hoc Mann-Whitney U test with Bonferroni correction for the IFNγRKO- chimeric groups.

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