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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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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2007
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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 |
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author | Nimmerjahn, Falk Ravetch, Jeffrey V. |
author_facet | Nimmerjahn, Falk Ravetch, Jeffrey V. |
author_sort | Nimmerjahn, Falk |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2118416 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21184162007-12-13 The antiinflammatory activity of IgG: the intravenous IgG paradox Nimmerjahn, Falk Ravetch, Jeffrey V. J Exp Med Commentaries 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. The Rockefeller University Press 2007-01-22 /pmc/articles/PMC2118416/ /pubmed/17227911 http://dx.doi.org/10.1084/jem.20061788 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Commentaries Nimmerjahn, Falk Ravetch, Jeffrey V. The antiinflammatory activity of IgG: the intravenous IgG paradox |
title | The antiinflammatory activity of IgG: the intravenous IgG paradox |
title_full | The antiinflammatory activity of IgG: the intravenous IgG paradox |
title_fullStr | The antiinflammatory activity of IgG: the intravenous IgG paradox |
title_full_unstemmed | The antiinflammatory activity of IgG: the intravenous IgG paradox |
title_short | The antiinflammatory activity of IgG: the intravenous IgG paradox |
title_sort | antiinflammatory activity of igg: the intravenous igg paradox |
topic | Commentaries |
url | 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 |
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