CCL21-induced T-cell adhesion to ICAM-1 and affinity/avidity regulation of LFA-1 depends on the ADAP/SKAP55 module. (A) Purified splenic WT and ADAP^−/− T cells were left untreated or stimulated with CCL21, anti–CD3 mAb 145-2C11 (TCR), PMA, or MnCl₂, respectively, and subsequently analyzed for their ability to bind plate-bound Fc-ICAM-1 (mean ± SD; n = 6 experiments). **P ≤ .001. n.s. indicates not significant. (B) Human primary T cells were transfected with either control siRNA (siC) or siRNAs against ADAP (siADAP). After 72 hours, cells were analyzed for their ability to bind soluble Fc-ICAM-1 in response to CCL21, anti-CD3 mAb OKT3 (TCR), or Mg²⁺/EDTA stimulation for 5 minutes. Suppression of ADAP expression was evaluated by flow cytometry. One representative experiment of 3 is shown. (C) Human T cells transfected as described in panel B were stimulated with CCL21, fixed, and stained with FITC-conjugated CD18 or CD11a antibodies. For each experiment, 30 randomly selected cells in triplicates were analyzed to calculate the percentage of cells with CD18 or CD11a clusters by confocal microscopy (mean ± SD; n = 4 experiments). *P ≤ .05.