Figure 2.
Figure 2. Specificity of the reactivity of rituximab with cyclic and linear peptides following their conjugation to KLH. Ninety-six-well polyvinyl-chloride microtiter plates were incubated with 50 μL of PBS solution containing KLH-cyclic peptides Rp15-C (○), Rp3-C (▵), and mRp3-C (⋄) (A-B) and linear peptides Rp1-L (♦), Rp5-L (▴), RpCD20-L (▪) (C-D) (5 μg/mL) for 12 hours at 4°C. After 2 washings and blockage of free protein-binding sites, a 4-fold serial dilution of rituximab (A,C) or infliximab (negative control; B,D) was added to the plate and their binding to peptide was detected with HRP-conjugated xeno-antibodies to human IgG (Fc portion). Bindings of rituximab to KLH-Qp1a (×) and to KLH (□) were included as negative controls.

Specificity of the reactivity of rituximab with cyclic and linear peptides following their conjugation to KLH. Ninety-six-well polyvinyl-chloride microtiter plates were incubated with 50 μL of PBS solution containing KLH-cyclic peptides Rp15-C (○), Rp3-C (▵), and mRp3-C (⋄) (A-B) and linear peptides Rp1-L (♦), Rp5-L (▴), RpCD20-L (▪) (C-D) (5 μg/mL) for 12 hours at 4°C. After 2 washings and blockage of free protein-binding sites, a 4-fold serial dilution of rituximab (A,C) or infliximab (negative control; B,D) was added to the plate and their binding to peptide was detected with HRP-conjugated xeno-antibodies to human IgG (Fc portion). Bindings of rituximab to KLH-Qp1a (×) and to KLH (□) were included as negative controls.

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