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. 2021 Feb 17;118(8):e2017213118. doi: 10.1073/pnas.2017213118

Fig. 2.

Fig. 2.

CD4+ T migration to gray matter is dependent on CXCR2 chemokine signaling in Type-B EAE mice. (A) Representative micrographs of CD4+ T cells in lumbar spinal cord sections labeled with CD4 antibody at 28 dpi (Left) and quantification of CD4+ T cell count in gray matter (GM), dGM, and vGM (Right) (Type-A EAE: n = 5; Type-B EAE: n = 4). (B) Representative confocal images with overlaid T cell trajectories (corresponding to 40 min of imaging) in vGM at 28 dpi. Average cell velocity (μm/min) is graphed (>30 cells analyzed per condition). Data are representative of two independent experiments. (C) Representative merged 3D micrograph of CD4+T cell (red) and Golgi-Cox–stained neuron (purple) in vGM of Type-B EAE lumbar spinal cord using conventional and reflection confocal modalities, respectively. (D) Representative merged 3D micrograph of fluorescent CD4+T cell and TUJ1+ neuron in ventral gray matter of Type-B EAE lumbar spinal cord. (E) Representative images (Left) and quantification (Right) of CD4+ T cells in vGM of the lumbar spinal cord of control Cxcr2 fl/fl and cCxcr2−/− mice at 28 dpi (n = 4 per condition). (F) Daily EAE disease scores of Type-B Cxcr2 fl/fl and cCxcr2−/− mice up to 28 dpi (Cxcr2 fl/fl: n = 8; cCxcr2−/−: n = 6). Statistical analysis: Mann–Whitney u test (A, B, and E), two-tailed Student’s t test (F). *P < 0.05.