The presence of gaps in the inflamed arthritic joint vasculature depends on platelets. (A) The platelet-depleting antibody or the isotype control antibody was injected to mice on day 0 and day 3. Arthritis was induced by injection of 75 μL of K/BxN serum on day 0 and day 2. On day 4, the 0.45-μm microspheres were intravenously injected in platelet (PLT)–depleted mice and control mice (with PLT), and the fluorescence was measured in ankle joints 5 minutes later. Nonarthritic mice were used as controls. Representative results are presented. ***P < .0001. (B) The signs of arthritis were monitored daily and presented as mean ± SEM. Arrow indicates parenteral administration of platelet-depleting antibody or isotypic control; and arrowheads, K/BxN serum administration. (C) Antibody injection, arthritis induction, microsphere injection, fluorescence measurements, controls, and results presentation were performed as in panel A. Mouse recombinant IL-1β was injected on days 0, 1, and 2 in mice receiving the platelet-depleting antibody. ***P = .0002 (top). ***P = .0001 (bottom). (D) The signs of arthritis were monitored as in panel B. Arrow indicates parenteral administration of platelet-depleting antibody or isotypic control; arrowheads, K/BxN serum administration; and double arrow, IL-1β administration.