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. Author manuscript; available in PMC: 2015 Mar 15.
Published in final edited form as: J Immunol. 2014 Feb 19;192(6):2837–2845. doi: 10.4049/jimmunol.1302484

Figure 6. CC-induced up-regulation of CD11b (CR3) and phagocytosis of CC are complement-mediated.

Figure 6

Whole blood pre-incubated with the complement inhibitors compstatin (Comp.), eculizumab (Eculiz.), C5a receptor antagonist (C5aR ant.), control peptide (Ctrl. Pep.) or anti-C7 (C7 antibody) was incubated with CC (3 × 107 particles/ml), or PBS/HSA. (A, B) Median fluorescent intensity (MFI) of CD11b on granulocytes and monocytes measured after 15 minutes. (C, D) Phagocytosis was determined based on shift in SSC induced by CC ingestion, as described in Materials and Methods. The decrease compared to the control peptide group in each panel (A-D) was significant (*, p < 0.05) for all comparisons, except for C7 antibody. Results are mean ± SEM, n=6. (E, F) Phagocytosis of CC in granulocytes and monocytes in whole blood from a C5 deficient donor (C5 def.), or C5 deficient donor reconstituted with purified C5 (50 µg/ml). Blood from three controls (Ctrl.) were analyzed in parallel. Results from the C5 deficient donor represent mean ± SD of two experiments performed at two time points.