Fig. 2.

CCR2, but not β7-integrin, mediates homing of circulating monocytes to the inflamed intestine. a Purified CD11b⁺Ly6C⁺ BM monocytes express CCR2, α4β7-integrin, and CCR9. Isotype controls are shown as gray shaded histogram. b Monocytes were purified from BM of CD45.2⁺ WT and gene-deficient donors (CCR2, β7-integrin, or CCR9), differentially labeled with either eFluor 450 or eFluor 670 and mixed at a 1:1 ratio. c Mixtures of labeled monocytes were transferred into non-manipulated and manipulated CD45.1⁺ CCR2^-/- recipients. Transferred cells were identified by congenic markers (left panel) and the donor monocytes identified as CD11b⁺CD11c^low/intCD64⁺ cells (middle panel). The frequency of the differentially labeled donor monocytes (right panel) was analyzed one day after cell transfer to determine the ratio of gene-deficient to WT cells. d In small intestinal lamina propria (siLP), colonic lamina propria (cLP), liver, spleen, and BM, the ratio of gene-deficient to WT monocytes was determined 1 day after cell transfer as indicated in c. Data are displayed as relative change with respect to control experiments comparing differentially labeled WT monocytes. Data were pooled from two or more independent experiments. Symbols depict individual mice, n = 4–7 mice. One-way ANOVA followed by Sidak’s multiple comparison tests; mean ± s.d.; ns not significant; *p < 0.05, **p < 0.01, ***p < 0.001