Requirement for FKN and its receptor, CX3CR1, in chemotaxis of macrophages to apoptotic cells. (A) Effect of anti-FKN neutralization on the activity of chemoattractants released from apoptotic cells. Chemotaxis of HMDM to Mutu-BL cells undergoing spontaneous or UV-induced apoptosis in the presence (■) or absence (▩) of neutralizing anti-FKN antibody (50 μg/mL) in the lower chamber. Chemotaxis is shown as fold increase above that of background (medium alone), which was set to 1. CCL5 (100 ng/mL) is included as a positive control. Data shown are mean plus or minus SEM of replicate high-power fields. Experiment shown is representative of 4 similar. Student t test (control vs anti-FKN treatment): ***P < .001. (B) Effect of exogenous FKN on macrophage chemotaxis to apoptotic cells. Chemotaxis of HMDM to Mutu-BL cells undergoing spontaneous or UV-induced apoptosis in the presence (■) or absence (▩) of exogenous recombinant human FKN (100 ng/mL) in the upper chamber. Experiment shown is representative of 6 similar. Student t test (control vs FKN treatment): ***P < .001. (C) Absence of FKN receptor CX3CR1 partially prevents macrophage chemotaxis to apoptotic cells. Chemotaxis of bone marrow–derived macrophages from wild-type (▩) or CX3CR1^−/− mice (■) toward cell-free supernatants of Mutu-BL cells at the indicated times after UV irradiation. C5a (6.25 ng/mL) is included as a positive control. Experiment shown is representative of 6. Student's t test (control vs anti-FKN cells): ***P < .001.