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. 2001 Nov 5;194(9):1361–1374. doi: 10.1084/jem.194.9.1361

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Copyright © 2001, The Rockefeller University Press

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Figure 3. — Monocytes home to inflamed PLNs via HEVs. Adoptive transfer of CX3CR1^+/GFP PBMCs into wild-type recipients was performed 5 d after induction of skin inflammation as described in Fig. 2. Draining PLNs were removed after 1 h and prepared for confocal microscopy using appropriate filters for detection of GFP⁺ monocytes (green) and HEVs, which were visualized using anti-PNAd mAb MECA-79 and Cy5-labeled anti–rat IgM (red). (A) Representative confocal micrographs of homed GFP⁺ monocytes in close proximity to MECA-79⁺ HEVs. (B) The frequency distribution of homed GFP⁺ monocytes relative to MECA-79⁺ HEVs and the subcapsular sinus was determined. Data are expressed as mean ± SEM of the percentage of GFP⁺ cells in each class. n = 90 random sections of five inflamed PLNs from two independent experiments.

Figure 3. — Monocytes home to inflamed PLNs via HEVs. Adoptive transfer of CX3CR1^+/GFP PBMCs into wild-type recipients was performed 5 d after induction of skin inflammation as described in Fig. 2. Draining PLNs were removed after 1 h and prepared for confocal microscopy using appropriate filters for detection of GFP⁺ monocytes (green) and HEVs, which were visualized using anti-PNAd mAb MECA-79 and Cy5-labeled anti–rat IgM (red). (A) Representative confocal micrographs of homed GFP⁺ monocytes in close proximity to MECA-79⁺ HEVs. (B) The frequency distribution of homed GFP⁺ monocytes relative to MECA-79⁺ HEVs and the subcapsular sinus was determined. Data are expressed as mean ± SEM of the percentage of GFP⁺ cells in each class. n = 90 random sections of five inflamed PLNs from two independent experiments.