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Correspondence
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Volume 341:57-58 July 1, 1999 Number 1
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Mechanism of Intravenous Immune Globulin Therapy

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 by Yu, Z.
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To the Editor: Yu and Lennon (Jan. 21 issue)1 present an intriguing hypothesis about how intravenous immune globulin ("IVIg") therapy works in autoimmune diseases. Another possibility is that simultaneous ligation of the Fc{gamma} receptor II and the B-cell receptor inhibits B-cell activation.2 Binding of the Fc{gamma} receptor II by the constant regions (Fc) of IgG molecules inhibits B-cell function through immune tyrosine inhibitory motifs (ITIM) on the cytoplasmic tail of the Fc{gamma} receptor II. This effect induces anergy or apoptosis3 of activated B cells. Such a system could regulate the quantity of IgG in the plasma. When the IgG concentration . . . [Full Text of this Article]

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