Fig. 1.
Fig. 1. Binding of FITC-labeled Gp96 to PMNs and monocytes. / PBLs (2 × 105) were incubated with Gp96-FITC (50 μg/mL) and analyzed by FACS gating on PMNs (CD66b+) or monocytes (CD14+). Gp96-FITC binding was competed in the presence of 5 times excess of unlabeled Gp96 on PMNs (A) or monocytes (C), but not by IgG2b as irrelevant protein (PMNs [B] or monocytes [D]). (E) The summarized results of normalized LPS-FITC or Gp96-FITC binding to PMNs from 4 independent experiments are presented with standard deviation. LPS-FITC or Gp96-FITC binding was competed using fucoidan (1 mg/mL), unlabeled LPS (5-fold), or Gp96 (5-fold) (*P < .004; **P < .05, by Student t test).

Binding of FITC-labeled Gp96 to PMNs and monocytes.

PBLs (2 × 105) were incubated with Gp96-FITC (50 μg/mL) and analyzed by FACS gating on PMNs (CD66b+) or monocytes (CD14+). Gp96-FITC binding was competed in the presence of 5 times excess of unlabeled Gp96 on PMNs (A) or monocytes (C), but not by IgG2b as irrelevant protein (PMNs [B] or monocytes [D]). (E) The summarized results of normalized LPS-FITC or Gp96-FITC binding to PMNs from 4 independent experiments are presented with standard deviation. LPS-FITC or Gp96-FITC binding was competed using fucoidan (1 mg/mL), unlabeled LPS (5-fold), or Gp96 (5-fold) (*P < .004; **P < .05, by Student t test).

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