Fig. 1.
Inhibition of IgG autoantibody activity by IVIgM. Increasing amounts of IVIgM (▵), IVIgM depleted of its rheumatoid factor activity (○), IVIg (□), a human monoclonal IgM rheumatoid factor (•), or monoclonal IgM (▴) were coincubated with a fixed amount of 125I-labeled affinity-purified anti-TG or anti-DNA IgG from 2 patients with Hashimoto's thyroiditis and 2 patients with SLE overnight at 4°C. The binding of 125I-IgG to the corresponding antigen was then assessed. (Left panels) inhibition of anti-TG activity; (right panels) inhibition of anti-DNA activity. The abscissa indicates molar ratios between competitor Ig and 125I-IgG autoantibody.

Inhibition of IgG autoantibody activity by IVIgM. Increasing amounts of IVIgM (▵), IVIgM depleted of its rheumatoid factor activity (○), IVIg (□), a human monoclonal IgM rheumatoid factor (•), or monoclonal IgM (▴) were coincubated with a fixed amount of 125I-labeled affinity-purified anti-TG or anti-DNA IgG from 2 patients with Hashimoto's thyroiditis and 2 patients with SLE overnight at 4°C. The binding of 125I-IgG to the corresponding antigen was then assessed. (Left panels) inhibition of anti-TG activity; (right panels) inhibition of anti-DNA activity. The abscissa indicates molar ratios between competitor Ig and 125I-IgG autoantibody.

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