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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: CD200-CD200R1 inhibitory signaling prevents spontaneous bacterial infection and promotes resolution of neuroinflammation and recovery after stroke

Fig. 5

Worsened stroke outcomes in CD200R1-deficient mice are associated with profound peripheral immune suppression 1 week after stroke. The percentage of circulating lymphocytes was significantly lower in CD200R1-knockout mice at 7 days after MCAO compared to wild-type littermate controls (a; N = 5/group). Stroke-induced lymphopenia was associated with an increase in the percentage of circulating CD4 T cells expressing the early T cell receptor (TCR) activation marker, CD69 (b, c), and those with effector memory (CD44hiCD62Llo) phenotype (d, e). A mouse vβ TCR screening panel containing 15 FITC-conjugated monoclonal antibodies was used to assess TCR vβ usage in CD4 T cells from the blood of CD200R1-deficient mice that underwent sham and stroke surgery. The mean percentage for each of the 15 subfamilies of T cell receptor vβ is displayed (f). Significant differences were found between the groups illustrating the narrowing of the CD4 TCR repertoire in CD200R1-knockout mice after MCAO (N = 5/group). Cell-specific FMO controls were used to determine positive gating. Asterisks adjacent to group labels designate a significant interaction between groups by two-way ANOVA. Error bars show mean SEM. KO knockout, WT wild-type, SH sham, ST stroke, SEM standard error of mean. *p < 0.05; **p < 0.01; ***p < 0.001

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