Figure 5
Figure 5. Contribution of Gi, integrin ligands, and RAPL to cell migration within the LN. (A) Lymphocyte movement in B-cell follicles observed by intravital microscopy of inguinal LN. Representative tracks of wild-type lymphocytes in recipient mice injected with control rat IgG (ct) (green), anti–ICAM-1 and anti–VCAM-1 mAbs (red), or pertussis toxin (blue). Representative tracks of RAPL-deficient lymphocytes (yellow) in untreated, normal recipient mice are shown. (B) Displacement and velocity profiles of wild-type and RAPL−/− lymphocytes in recipient mice shown in panel A. Fifty-nine cells were tracked for 10 minutes for each dataset. The velocity data were obtained from movements measured every 30 seconds. (C) Median displacement and velocity of populations shown in panel B. Statistical significance was determined by a t test. *P < .001 compared with lymphocytes in rat IgG-administered recipient mice.

Contribution of Gi, integrin ligands, and RAPL to cell migration within the LN. (A) Lymphocyte movement in B-cell follicles observed by intravital microscopy of inguinal LN. Representative tracks of wild-type lymphocytes in recipient mice injected with control rat IgG (ct) (green), anti–ICAM-1 and anti–VCAM-1 mAbs (red), or pertussis toxin (blue). Representative tracks of RAPL-deficient lymphocytes (yellow) in untreated, normal recipient mice are shown. (B) Displacement and velocity profiles of wild-type and RAPL−/− lymphocytes in recipient mice shown in panel A. Fifty-nine cells were tracked for 10 minutes for each dataset. The velocity data were obtained from movements measured every 30 seconds. (C) Median displacement and velocity of populations shown in panel B. Statistical significance was determined by a t test. *P < .001 compared with lymphocytes in rat IgG-administered recipient mice.

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