Model depicting the role of the LTB₄–BLT1 axis in promoting neutrophil arrest and extravasation in vivo. Under control conditions, neutrophils respond to inflammatory cues by releasing EVs that relay LTB₄ signals in an autocrine/paracrine manner. The LTB₄–BLT1 axis triggers the redistribution of NMIIA and Itgb2 for sustained arrest in the inflamed vessel, followed by extravasation into the interstitium. These mechanisms are impaired in Alox5^−/− or Blt1^−/− neutrophils, resulting in their reduced arrest and extravasation in response to inflammation. The specific mechanisms regulating the release of LTB₄ from EVs and the local action of LTB₄ in the inflamed vessels have yet to be determined.