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Immune complexes as therapy for autoimmunity
Raphael Clynes
Raphael Clynes
Published January 3, 2005
Citation Information: J Clin Invest. 2005;115(1):25-27. https://doi.org/10.1172/JCI23994.
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Commentary

Immune complexes as therapy for autoimmunity

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Abstract

For several decades, intravenous Ig has been used as treatment for a variety of immune-related diseases, including immune thrombocytopenic purpura (ITP), autoimmune neuropathies, systemic lupus erythematosus, myasthenia gravis, Guillain-Barré syndrome, skin blistering syndromes, and Kawasaki disease. Despite years of use, its mechanism of immunomodulation is still unclear. Recent studies using mouse models of ITP and arthritis, including one reported in this issue of the JCI, now provide some insights into this mechanism and the rationale for the development of Fcγ receptor–targeted therapeutics.

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Raphael Clynes

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Figure 1

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Inhibition of phagocytosis in vivo can be accomplished via IC-mediated i...
Inhibition of phagocytosis in vivo can be accomplished via IC-mediated inhibition of FcγR functional activity. These complexes, varying in size and valency, operate through distinct mechanistic pathways. IVIg leads to the formation of variably sized ICs, including small monomeric and dimeric complexes. The small ICs (Ig dimers or soluble antigen/donor Ig complexes) require CSF-1–dependent macrophages and FcγRII expression to mediate their as-yet-undefined anti-inflammatory effect. Intravenous anti-D generates large particulate ICs, namely opsonized rbcs. These large ICs induce a phagocytic block in vivo in a manner independent of FcγRII expression. Perhaps mimicking the situation directly, antibodies that specifically engage either the inhibitory FcγRII (4) or the activating FcγRIII (4, 5) can also induce platelet count recovery.
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