CX₃CR1 expression regulates both Th1- and Th2-induced skin inflammation. (A) CSFE-labeled CX₃CR1^+/+ WT15 Thy1.1^+/+ CD4⁺ T cells were injected i.v. into CX₃CR1^gfp/gfp or CX₃CR1^+/gfp mice 1 d before epicutaneous sensitization with LACK. Donor cells were analyzed by flow cytometry 5 d later in inguinal LNs after gating onto CD4⁺ Thy1.1⁺ cells. Data show one representative flow cytometry profile of CFSE staining with numbers indicating frequencies of dividing donor cells ± SEM (n = 6). (B) CSFE-labeled CX₃CR1^+/gfp Thy1.1^+/− and CX₃CR1^gfp/gfp Thy1.1^+/+ WT15 CD4⁺ T cells were coinjected i.v. into WT Thy1.1^−/− Thy1.2^+/+ mice 1 d before LACK or PBS epicutaneous sensitization. Donor cells were analyzed by flow cytometry 4 d later in inguinal LNs after gating CD4⁺ Thy1.1⁺ cells. Data show a representative flow cytometry profile of CFSE staining with numbers indicating dividing CX₃CR1^+/+ and CX₃CR1^gfp/gfp donor cells (n = 5 mice in each group). (C and D) WT mice were injected at day −1 with LACK-specific CX₃CR1^gfp/gfp or CX₃CR1^+/gfp Th1 or Th2 cells, sensitized for one single week with LACK or PBS at day 0, and further analyzed at day 7. (C) Epidermal thickness. (D) Eosinophil and mast cell numbers in dermis at the site of sensitization. Data are expressed as mean ± SEM (n = 6–10 animals per group). One out of two independent experiments is shown for each panel. *, P < 0.05.