B7-H1 restricts spontaneous CNS autoimmunity and prevents T-cell infiltration into the brain of sick OSE mice. (A) Percentages of OSEWT and OSEKO mice that spontaneously developed EAE symptoms over a period of 12 wk after birth. Forty-five OSEWT and 57 OSEKO mice were analyzed. (B) Survival of 246 OSEWT and 216 OSEKO mice was monitored over a period of 140 d after birth. Mice were recorded as dead when they reached the clinical score 5.5 or higher; mice eliminated for reasons unrelated to disease course (all with score below 5.5) were censored (indicated by vertical ticks). (C) Clinical scores of 18 OSEWT and 18 OSEKO mice until 70 d of age. (D–F) Immunohistochemical analysis of T-cell infiltration in different CNS regions of 12 OSEWT and 10 OSEKO mice (score-matched, mean clinical score 5.75). (D) Representative images of T-cell infiltrates in the spinal cord, corpus callosum, and cerebellum, as indicated. (E) Quantification of the extent of inflammation and T-cell infiltration in the spinal cord parenchyma and leptomeninges, as indicated (Top and Middle); semiquantitative scores of T-cell infiltration in the cerebellum and brainstem, and in the cerebrum (Bottom). (F) Representative images of T-cell infiltration in different brain areas of OSEWT and OSEKO mice. (D and F) T cells are indicated by arrowheads. The asterisk in F indicates a postcapillary venule. (Scale bars: D, spinal cord, 200 μm; corpus callosum, 100 μm; cerebellum, 200 μm; F, 100 μm.) (E) Each data point represents one mouse. (A and B) Log-rank (Mantel–Cox) test. (C) Two-way ANOVA with Bonferroni correction for multiple comparisons. (E) Unpaired, two-tailed Student’s t test. *P < 0.05; ***P < 0.001; ns, not significant.