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. Author manuscript; available in PMC: 2017 Jun 21.
Published in final edited form as: Immunity. 2016 Jun 14;44(6):1271–1283. doi: 10.1016/j.immuni.2016.05.013

Figure 7. Critical role of the OX40-RelB pathway in suppression of EAE in vivo.

Figure 7

(A) Incidence and clinical scores of EAE in Ifng−/− mice treated with OX86 or IgG. Data are presented as mean ± SD (n=7). ** p <0.01.

(B) Tissue pathology of spinal cord sections in Ifng−/− mice. Arrowhead indicates inflammatory cell infiltration (H&E) and area of severe demyelination. Bar scale: 100μm.

(C and D) FACS plots showing IL-17+CD4+ T cells obtained from the central nervous system (CNS) (C). Summaries of relative percentage (left) and absolute numbers (right) of IL-17-producing CD4+ cells in the CNS (D). Data are presented as mean ± SD (n=3). ** p <0.01.

(E) Incidence and clinical scores of EAE in Rag1−/− mice adoptively transferred with WT or Relb−/− CD4+ T cells. Data are presented as mean ± SD (n=5 and 7). ** p <0.01.

(F and G) Tissue histology of spinal cord sections. Arrowheads indicate inflammatory cell infiltration (H&E) (F), and areas of severe demyelination (Luxol fast blue, LFB) (G). Bar scale: 100μm.

(H) FACS plots showing IL-17-producing CD4+ T cells obtained from CNS of host mice. (I) The graph shows relative percentage and absolute numbers of IL-17-producing CD4+ cells in the CNS. Data are presented as mean ± SD of 3 experiments (n=3). ** p <0.01.