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. 2009 Apr 20;119(5):1286–1297. doi: 10.1172/JCI38399

Figure 7. Interaction between kidney DCs and Th cells causes intrarenal CTL accumulation.

Figure 7

NOH (black bars) or non-Tg (white bars) mice were injected with 5 × 106 OT-I cells alone or together with 5 × 106 activated OT-II cells. (A–C) After 7 days, single-cell suspensions of the kidney (A and B) or the spleen (C) were analyzed by flow cytometry to determine numbers of CD8+Vα2+Vβ5+ OT-I (A and C) or proportions of (B) IFN-γ–producing OT-I cells. (D) Numbers of CD4+ Vα2+Vβ5+ OT-II cells were determined after injection of 5 × 106 OT-II cells alone or together with 5 × 106 activated OT-II cells. (E) Experiments depicted in A–C show determination of Ki-67+ OT-I cells. In vitro–activated OT-II cells served as positive control, naive OT-II cells as negative control for proliferating cells. (F and G) Vα2+Vβ5+CD4+ OT-II (F) or Vα2+Vβ5+CD8+ OT-I cells (G) were sorted from kidney cell suspensions of experiments depicted in A–C. mRNA encoding CCL3, CCL4, CCL5, and CCR5 was determined, and the ratio between cells from NOH and non-Tg controls was displayed. (H) Mononuclear cell infiltrates and noninfiltrated tubulointerstitial control areas were excised from kidney cryosections as shown in Supplemental Figure 8. mRNA encoding CCL3, CCL4, CCL5, and CCR5 was determined, and the ratio between infiltrates from injected NOH and non-Tg controls was displayed. Results are representative of 2 experiments. *P < 0.05; **P < 0.01; ***P < 0.001. Data are presented as mean ± SD.