Fig. 1.
Fig. 1. Neutrophil binding of 125I-labeled antibodies. Neutrophils (1 × 106) from the patient and 2 normal donors, unactivated (control, ▪) or activated with the combination of TNF- and fMLP (TNF/fMLP, ), were incubated with125I-labeled antibodies against L-selectin, CD18, and PECAM-1 in a 96-well plate. The expression of these cell adhesion molecules was assessed by the binding of labeled antibody as determined by the total counts per well of cells. The expression of L-selectin, CD18, and PECAM-1 on the patient’s neutrophils were comparable with the expression found on neutrophils from normal control donors and stimulation with TNF- and fMLP decreased the expression of L-selectin and increased the surface level of CD18 as has been previously reported. These data are representative of 3 experiments done in triplicate in which the patient was compared with 2 normal donors and in which different normal donors were used in each experiment.

Neutrophil binding of 125I-labeled antibodies. Neutrophils (1 × 106) from the patient and 2 normal donors, unactivated (control, ▪) or activated with the combination of TNF- and fMLP (TNF/fMLP, ), were incubated with125I-labeled antibodies against L-selectin, CD18, and PECAM-1 in a 96-well plate. The expression of these cell adhesion molecules was assessed by the binding of labeled antibody as determined by the total counts per well of cells. The expression of L-selectin, CD18, and PECAM-1 on the patient’s neutrophils were comparable with the expression found on neutrophils from normal control donors and stimulation with TNF- and fMLP decreased the expression of L-selectin and increased the surface level of CD18 as has been previously reported. These data are representative of 3 experiments done in triplicate in which the patient was compared with 2 normal donors and in which different normal donors were used in each experiment.

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