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Fig. 2 | Arthritis Research & Therapy

Fig. 2

From: Depletion of activated macrophages with a folate receptor-beta-specific antibody improves symptoms in mouse models of rheumatoid arthritis

Fig. 2

Characterization of anti-human FR-β (m909) and anti-mouse FR-β (F3) mAbs. a Shift in fluorescence intensity of CHO-β cells determined in the presence of increasing concentrations of m909 by flow cytometry. b m909-mediated ADCC of CHO-β cells incubated in the presence of different effector (human PBMCs) to target cell (CHO-β cells) ratios. ADCC-mediated CHO-β cell lysis was measured after 24 h by a LDH release assay. c m909-mediated ADCC of M1- or M2-like macrophages by PBMC effector cells. Isolated human PBMCs were differentiated into M1- or M2-like macrophages and activated to express FR-β as described in the Materials and methods section. After macrophage opsonization with m909 (target cells), freshly isolated human PBMCs (effector cells) were added to the macrophage culture, and ADCC-mediated lysis was measured after 24 h via LDH release assay. d m909-mediated CDC of CHO-β cells incubated in the presence of fresh human plasma. CHO-β cells, m909, and human serum diluted in RPMI1640 medium were incubated for 3 h at 37 °C. Cell lysis was determined via LDH release assay. e Shift in fluorescence intensity of RAW 264.7 cells determined in the presence of increasing concentrations of F3 by flow cytometry. f F3-mediated ADCC of RAW 264.7 cells using a commercially available murine ADCC luminescence reporter bioassay. All error bars represent standard deviation for all panels

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