Supplementary Figure 8: Phenotypic characterization of the lymphocyte homing defect. | Nature Neuroscience

Supplementary Figure 8: Phenotypic characterization of the lymphocyte homing defect.

From: Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex

Supplementary Figure 8

Homing of injected donor splenocytes (composed of ~52% CD19+, ~23% CD4+, ~17% CD8+ cells) was not equally impaired for all donor cell populations or target organs. (a) The homing deficit was most pronounced for B cells with reduced percentage of CD19+ cells (only 30% B cells after SCI compared to almost 60% after sham), while the percentage of T cells in the donor population was increased (despite total reduction). (b) In contrast, homing of donor cells to the cervical LNs was equally impaired for all cell populations after SCI. (c) The 2-hour homing deficit of donor cells to most organs was detectable already 1 d post SCI, most pronounced to peripheral LNs. (d) Not only homing, but also redistribution of donor cells (15 hours cell migration) was severely disturbed after SCI. Data are mean ± SEM, n=3-5 (a-b) or 3 (c-d) animals per group. * p<0.05; ** p<0.01; *** p<0.001, unpaired Student’s t test (a-b) or 1-way ANOVA with Tukey’s multiple comparison test (c-d).

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