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. 2013 Sep 3;123(10):4242–4254. doi: 10.1172/JCI70143

Figure 3. CX3CR1 deficiency reduces intrarenal Th1 response and improves kidney function.

Figure 3

(A) Absolute numbers of IFN-γ–producing CD4+ T cells and (B) of TNF-producing DCs and MPs per kidney of CX3CR1GFP/+ reporter mice and CX3CR1GFP/GFP-deficient mice 10 days after NTN induction, as determined by intracellular flow cytometry. In A, cell numbers in 4 individual experiments were given as percentage of the mean cell number in the CX3CR1-competent groups. (C) Creatinine clearance in CX3CR1GFP/+ and CX3CR1GFP/GFP mice 10 days after NTN induction. (D) Blood urea nitrogen in CX3CR1+/+ and CX3CR1GFP/GFP mice 10 days after NTN induction. (E) Albumin excretion normalized to creatinine by CX3CR1GFP/+ and CX3CR1GFP/GFP mice 10 days after NTN induction. Urine was collected for 12 hours. Data points represent individual mice, and results (AC) are combined from 2 to 4 individual experiments, with 2 to 5 mice per group, or (D and E) are representative of 2 individual experiments, with 10 mice per group. Statistical significance was tested with the 2-tailed Mann-Whitney test.