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. 2001 Apr 16;193(8):967–974. doi: 10.1084/jem.193.8.967

Figure 1.

Figure 1

CD40 is critical for the induction of active MOG-EAE in C57BL/6 mice and T cell priming. (A) Early administration of anti-CD154 blocks the development of MOG-induced EAE. Mice were immunized with MOG35–55 in CFA and given 350 μg/mouse of anti-CD154 mAbs three times per week starting at the time of immunization (▵). Control mice were treated with H-Ig mAbs (♦; n = 6/group). (B) CD40−/− mice are not susceptible to MOG-induced EAE. CD40−/− (□) and CD40+/+ (♦) mice were immunized as described in panel A, and disease was monitored (n = 9/group). (C) Treatment of mice with anti-CD154 at disease onset ameliorated MOG-induced EAE. Mice were treated at the first sign of clinical disease with either anti-CD154 (▵) or control H-Ig (♦) (n = 9/group). (D) T cell priming to MOG is reduced in CD40−/− mice. To assess the ability of CD40−/− mice to prime T cells against MOG35–55, CD40+/+ (+/+) or CD40−/− (−/−) mice were immunized with MOG35–55 in CFA. LN cells were harvested after 5 d and stimulated with either no antigen, 100 μg of MOG35–55, or irrelevant PLP peptide. (E) MOG-induced IFN-γ secretion is reduced in CD40−/− mice. IFN-γ production from LN cells primed to MOG35–55 in CD40+/+ and CD40−/− was assessed in vitro as described in D. Displayed is a representative of at least three experiments.