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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| Format: | Online |
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The Rockefeller University Press
2007
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118416/ |
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pubmed-21184162007-12-13 The antiinflammatory activity of IgG: the intravenous IgG paradox Nimmerjahn, Falk Ravetch, Jeffrey V. 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/). |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Nimmerjahn, Falk Ravetch, Jeffrey V. |
| spellingShingle |
Nimmerjahn, Falk Ravetch, Jeffrey V. The antiinflammatory activity of IgG: the intravenous IgG paradox |
| author_facet |
Nimmerjahn, Falk Ravetch, Jeffrey V. |
| author_sort |
Nimmerjahn, Falk |
| title |
The antiinflammatory activity of IgG: the intravenous IgG paradox |
| title_short |
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_sort |
antiinflammatory activity of igg: the intravenous igg paradox |
| 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. |
| publisher |
The Rockefeller University Press |
| publishDate |
2007 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118416/ |
| _version_ |
1611414745698533376 |