CCR2⁺ monocytes transition into CCR2⁺CX₃CR1⁺ monocytes at a site of sterile injury in the liver. (a and b) Conversion of RFP⁺ monocytes to RFP⁺GFP⁺ monocytes 48 h after focal liver injury in Ccr2^RFP/+/Cx3cr1^GFP/+ mice (a) or Ccr2^RFP/+/Cx3cr1^GFP/+ mice treated with anti–IL-4 and anti–IL-10-blocking antibodies (b). (c and d) Quantification of the percentage of each image corresponding to each of denoted hue in Ccr2^RFP/+/Cx3cr1^GFP/+ mice (c) or Ccr2^RFP/+/Cx3cr1^GFP/+ mice treated with anti–IL-4 and anti–IL-10 blocking antibodies (d). (e and f) Clearance of cellular debris 48 h after injury in control mice (e) and in anti–IL-4– and anti–IL-10–treated mice (f). (g) Quantification of dead cells (measured by percentage of area covered by Sytox green) within the lesion 48 h after injury. Bars, 200 µm; data are representative of three independent experiments. (h and i). Representative images of collagen in the liver of WT mice 72 h after focal injury. Mice treated with either an isotype control antibody (h) or anti–IL-4 and anti–IL-10-blocking antibodies (i). Injury border delineated with a dashed white line. (j) Quantification of collagen deposition within the burn 72 h after injury. Values expressed as a percentage of burn area covered by collagen. n > 3 mice per group; error bars, SEM. (h–j) Data representative of two independent experiments.