The hem1−/− DC–T cell priming defect is mediated by the pERM–ICAM1–LFA-1 axis.(A) Western blots for ERM, pERM, and GAPDH in mature WT and hem1−/− DCs, representative example of three biological replicates. (B) Relative intensity of pERM signal in mature WT and hem1−/− DCs, t test, three biological replicates. (C) Schematic overview of AFM setup for tether pulling. (D) Static tether force for mature WT and hem1−/− DCs, two biological replicates, t test. (E) Percentages of activated β2-integrin–deficient T cells assessed by CD62L/CD69 surface expression at indicated OVA323-339 peptide concentrations, three biological replicates, mean ± SD. Data were tested for normal distribution, transformed if necessary, and tested by using Student’s t test. ns, not significant. *, P ≤ 0.05; ***, P ≤ 0.001.
Figure 5.

The hem1−/− DC–T cell priming defect is mediated by the pERM–ICAM1–LFA-1 axis. (A) Western blots for ERM, pERM, and GAPDH in mature WT and hem1−/− DCs, representative example of three biological replicates. (B) Relative intensity of pERM signal in mature WT and hem1−/− DCs, t test, three biological replicates. (C) Schematic overview of AFM setup for tether pulling. (D) Static tether force for mature WT and hem1−/− DCs, two biological replicates, t test. (E) Percentages of activated β2-integrin–deficient T cells assessed by CD62L/CD69 surface expression at indicated OVA323-339 peptide concentrations, three biological replicates, mean ± SD. Data were tested for normal distribution, transformed if necessary, and tested by using Student’s t test. ns, not significant. *, P ≤ 0.05; ***, P ≤ 0.001.

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