Infarct volumes and functional outcomes 24 hours after focal cerebral ischemia in WT mice, RAG1−/− mice lacking T cells and B cells, RAG1−/− mice reconstituted with B cells or CD3+ T cells, TCR-transgenic mice bearing only a single CD8+ (2C/RAG2, OTI/RAG1) or CD4+ (OTII/RAG1, 2D2/RAG1) TCR clone of defined specificity, mice lacking essential counterreceptors of TCR costimulation (CD28−/−, B7-H1−/−, and PD1−/−), CD1d−/− (devoid of NKT cells), and γδ T cell–deficient mice. (A) Brain infarct volumes from the different animals groups indicated 24 hours after tMCAO as measured by planimetry (n = 10 per group, except for RAG1−/− mice reconstituted with CD3+ T cells: n = 5). Note that RAG1−/− mice developed significantly smaller strokes compared with wild-type (WT) controls, while no significant differences (ns) in infarct volumes were observed between RAG1−/− mice and RAG1−/− mice reconstituted with B cells. In contrast, reconstitution of RAG1−/− mice with CD3+ T cells rescued the phenotype and infarct volumes, and functional deficits returned to WT levels. (B) Top panel shows neurologic Bederson score and bottom panel shows grip test from the different groups indicated as assessed at day 1 after tMCAO (n = 10 per group, except for RAG1−/− mice reconstituted with CD3+ T cells: n = 5). *P < .05 and **P < .001, Bonferroni-corrected 1-way ANOVA compared with WT controls. Error bars represent SD.