Blocking inflammatory macrophages migration marginally impaired their clearance during resolution. (A) Heat map showing the expression of chemotactic receptors in MHC-II⁻ and MHC-II⁺ inflammatory macrophages 5 days after intraperitoneal administration of thioglycollate (3 replicates were generated for each population). (B) Kinetics of MHC-II⁻ and MHC-II⁺ inflammatory macrophages during the course of thioglycollate-induced peritonitis in CCR7-deficient mice and controls (n = 5 mice per group per time). (C) Accumulation of inflammatory macrophage in the mediastinal LN of CCR7-deficient mice and controls 5 days after intraperitoneal administration of thioglycollate (n = 5 mice per group). (D) Mobilization to the mediastinal LN of adoptively transferred F4/80⁺ CD36⁺ CD45.1⁺ inflammatory macrophages in CD45.2 mice injected with thioglycollate in the presence of PTX or iPTX (n = 5-7 per group). To maximize the recovery, cells and PTX or iPTX (single injection) were injected in the peritoneum at day 2, and LNs were analyzed at day 5. (E) Baseline number of inflammatory macrophage in the peritoneum at day 5 and numbers of macrophages recovered at day 8 after treatment with either active (PTX) or inactive (iPTX) pertussis toxin at day 5. Each symbol represents one mouse. (F) The number of F4/80⁺CD36⁺ macrophages recovered in the mediastinal LN at day 8 from the experiment in panel E, illustrating that active pertussis toxin prevented emigration to the LN.