Figure 3
Figure 3. Role of β2 and α4 integrins as well as PECAM-1, ICAM-1, ICAM-2, and VCAM-1 for CCL3-elicited leukocyte responses. (A-B) Leukocyte rolling, (C-D) firm adherence, and (E-F) transmigration were quantified in postcapillary venules of the cremaster muscle using RLOT in vivo microscopy as detailed in “Quantification of leukocyte kinetics and microhemodynamic parameters.” Panels show results for PBS-treated WT control mice as well as for WT mice receiving blocking mAbs directed against LFA-1, Mac-1, α4 integrins, PECAM-1 (clone Mec13.3), ICAM-1, ICAM-2, and VCAM-1 or isotype control and a nonblocking anti-PECAM-1 mAb (clone 390) after stimulation with CCL3 (mean ± SEM for n = 4 per group; #P < .05, vs unstimulated; *P < .05, vs isotype control).

Role of β2 and α4 integrins as well as PECAM-1, ICAM-1, ICAM-2, and VCAM-1 for CCL3-elicited leukocyte responses. (A-B) Leukocyte rolling, (C-D) firm adherence, and (E-F) transmigration were quantified in postcapillary venules of the cremaster muscle using RLOT in vivo microscopy as detailed in “Quantification of leukocyte kinetics and microhemodynamic parameters.” Panels show results for PBS-treated WT control mice as well as for WT mice receiving blocking mAbs directed against LFA-1, Mac-1, α4 integrins, PECAM-1 (clone Mec13.3), ICAM-1, ICAM-2, and VCAM-1 or isotype control and a nonblocking anti-PECAM-1 mAb (clone 390) after stimulation with CCL3 (mean ± SEM for n = 4 per group; #P < .05, vs unstimulated; *P < .05, vs isotype control).

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