SSG does not potentiate neutrophil ADCC solely through the inhibition of SHP-1. (A) Dose-dependent inhibition of human recombinant SHP-1 by SSG (4 independent experiments were performed in triplicate). (B) Neutrophil ADCC toward Raji CD47KO cells opsonized with rituximab in the absence or presence of SSG or increasing concentrations (1.6, 16, or 80 µM) of cefsulodin (n = 4 donors from 2 independent experiments). (C) Inhibition of human recombinant SHP-1 by 20 µM 2-iodoacetamide (2-iod; maximum inhibition), increasing concentrations (12.5 or 100 µM) of SSG and increasing concentrations (20, 40, or 60 µM) of cefsulodin (6 independent experiments were performed in triplicate). Statistics indicate the comparison between 2-iodoacetamide and the different concentrations of SSG and cefsulodin. (D) Neutrophil ADCC of Raji wild type or CD47KO cells with 4 healthy neutrophil donors (closed symbols, left) and 1 SHP-1–deficient patient on 2 separate occasions (open symbols, right). Raji cells were opsonized with rituximab and neutrophils were incubated with or without SSG. Note that SHP-1–deficient neutrophils show high killing under basal conditions, which is further enhanced with SSG. Data shown is from 2 independent experiments. Data are mean ± SEM. *P ≤ .05; **P ≤ .01. IC₅₀, 50% inhibitory concentration; PBS, phosphate-buffered saline.