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. 2014 Sep 26;9(9):e107772. doi: 10.1371/journal.pone.0107772

Figure 2. Complement deposition on ganglioside-coated microtiter plates using anti-GM1 IgM (n = 6), anti-GM1 (n = 8) or anti-GQ1b (n = 11) IgG antibodies from patients with multifocal motor neuropathy, Guillain–Barré or Miller Fisher syndrome (total 25 samples).

Figure 2

All patients’ sera were diluted (1∶100) and complement source was diluted (1∶100). C3 and C4 deposition were measured as optical densities (OD) at 492 nm. Each sample’s C3 and C4 deposition OD were plotted and correlation coefficient was calculated (A). Intravenous immunoglobulin (IVIG) inhibited the classical complement pathway. Patients’ serum diluted (1∶100), complement source diluted (1∶100) and IVIG (10 mg/mL) or human serum albumin (HSA, 10 mg/mL; control) were treated. C3 and C4 deposition were measured as optical densities (OD) at 492 nm. The results were normalized to the HSA treated C3 deposition OD, and showed as % of control (B).