Lack of involvement of FcαRI in monocyte–mediated trogocytosis of RBCs sensitized with e-IgA autoantibodies. (A-B) PBMCs were incubated with PKH67-labeled RBCs, left untreated or sensitized with e-IgA autoantibodies and the acquisition of PKH67 fluorescence by CD14⁺ monocytes was determined before (T0) and after 90 minutes (T90) of coculture. Eluted IgA autoantibodies were used pure or diluted 1:10 in Hanks buffered salt solution (n = 3). *P < .05 vs e-IgA–treated; U test. (C-D) Before incubation with RBCs, PBMCs were treated either with a polyspecific FcR blocking reagent (FcR blocker; n = 6) or with the My43–specific FcαRI/CD89 blocking antibody (50 μg/mL; n = 4); ns: not significantly different vs nontreated monocytes; t test. (E-F) PBMCs incubated with mAb against RhD-sensitized RBCs (mIgG anti-RhD; n = 3) were tested for trogocytosis after treatment with the FcR Blocker. **P < .01 vs untreated monocytes; 2-tailed paired t test. The events shown are gated on monocytes, based on forward scatter/side scatter parameters and CD14 staining. Data were collected on a BD FACScan cytometer and analyzed with CellQuest Pro software Version 4.0. Dot plots (left panels A,C,E) show the results from one representative experiment. The numbers indicate the mfi of the gated populations. Histograms (right panel B,D,F) show means and standard errors of the means from at least 3 independent determinations. The histograms in panel B show the mfi values. The histograms in panels D and F show the inhibition index for fluorescence transferred to CD14⁺; the value obtained for sensitized RBCs incubated with untreated monocytes represent 100%.