The antiinflammatory activity of IgG: the intravenous IgG paradox

How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved. We have recently shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that is modified with terminal sialic acids on their Fc-linked glycans. Here we propose that these...

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Detalles Bibliográficos
Autores principales: Nimmerjahn, Falk, Ravetch, Jeffrey V.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Commentaries
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118416/
https://www.ncbi.nlm.nih.gov/pubmed/17227911
http://dx.doi.org/10.1084/jem.20061788
Descripción
Sumario:How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved. We have recently shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that is modified with terminal sialic acids on their Fc-linked glycans. Here we propose that these Fc-sialylated IgGs engage a unique receptor on macrophages that, in turn, leads to the upregulation of an inhibitory Fcγ receptor (FcγR), thereby protecting against autoantibody-mediated pathology.

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