Fig. 5

Immune cell composition in infarcts at the stage of liquefactive necrosis in humans and mice. a Representative images of CD3+ T-lymphocyte, CD20+ B-lymphocyte, and CD68+ macrophage/microglia infiltration in human infarcts at the stage of liquefactive necrosis. Scale bars, 10 μm (human, CD3 and CD20 images) and 30 μm (human, CD68 image). b Quantification of CD4+ and CD8+ T-lymphocyte, and CD20+ B-lymphocyte infiltration into the infarcts. c Representative images of CD3+ T-lymphocytes, B220+ B-lymphocytes, and CD68+ macrophages/microglia in the infarcts of C57BL/6 and BALB/c mice at 7 weeks post-stroke. Scale bar,100 μm. d Higher magnification images of CD68+ macrophages/microglia in the infarct to reveal individual cells. Scale bar, 25 μm. e Quantification of CD3+ T-lymphocyte infiltration, B220+ B-lymphocyte infiltration, and CD68 immunostaining in mouse infarcts. ****p < 0.0001 compared to week 1, +++ p < 0.001 compared to BALB/c, ++++ p < 0.0001 compared to BALB/c. f Flow cytometry on cells gated by CD4, using markers of Th1 cells (T-bet and IFNγ), demonstrates that at 7 weeks post-stroke, the CD4+ T cell response in the infarct in C57BL/6 mice is more polarized towards a Th1 response than in BALB/c mice. g Flow cytometry on cells gated by CD4, using markers of Th2 cells (STAT6 and IL-4), demonstrates that at 7 weeks post-stroke, the T cell response in the infarct in BALB/c mice is more polarized towards a Th2 response than in C57BL/6 mice. h There were few CD4+ IL-17+ cells detected in the infarct of both strains. i There were no CD4+ Foxp3 cells detected in the infarct in either strain. j Table showing the % CD4 lymphocytes positive for each marker