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Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies

The biological activities of human IgG antibodies predominantly rely on a family of receptors for the Fc portion of IgG, FcγRs: FcγRI, FcγRIIA, FcγRIIB, FcγRIIC, FcγRIIIA, FcγRIIIB, FcRL5, FcRn, and TRIM21. All FcγRs bind IgG at the cell surface, except FcRn and TRIM21 that bind IgG once internalize...

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Autores principales: Gillis, Caitlin, Gouel-Chéron, Aurélie, Jönsson, Friederike, Bruhns, Pierre
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038777/
https://www.ncbi.nlm.nih.gov/pubmed/24910634
http://dx.doi.org/10.3389/fimmu.2014.00254
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author Gillis, Caitlin
Gouel-Chéron, Aurélie
Jönsson, Friederike
Bruhns, Pierre
author_facet Gillis, Caitlin
Gouel-Chéron, Aurélie
Jönsson, Friederike
Bruhns, Pierre
author_sort Gillis, Caitlin
collection PubMed
description The biological activities of human IgG antibodies predominantly rely on a family of receptors for the Fc portion of IgG, FcγRs: FcγRI, FcγRIIA, FcγRIIB, FcγRIIC, FcγRIIIA, FcγRIIIB, FcRL5, FcRn, and TRIM21. All FcγRs bind IgG at the cell surface, except FcRn and TRIM21 that bind IgG once internalized. The affinity of FcγRs for IgG is determined by polymorphisms of human FcγRs and ranges from 2 × 10(4) to 8 × 10(7) M(−1). The biological functions of FcγRs extend from cellular activation or inhibition, IgG-internalization/endocytosis/phagocytosis to IgG transport and recycling. This review focuses on human FcγRs and intends to present an overview of the current understanding of how these receptors may contribute to various pathologies. It will define FcγRs and their polymorphic variants, their affinity for human IgG subclasses, and review the associations found between FcγR polymorphisms and human pathologies. It will also describe the human FcγR-transgenic mice that have been used to study the role of these receptors in autoimmune, inflammatory, and allergic disease models.
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spelling pubmed-40387772014-06-06 Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies Gillis, Caitlin Gouel-Chéron, Aurélie Jönsson, Friederike Bruhns, Pierre Front Immunol Immunology The biological activities of human IgG antibodies predominantly rely on a family of receptors for the Fc portion of IgG, FcγRs: FcγRI, FcγRIIA, FcγRIIB, FcγRIIC, FcγRIIIA, FcγRIIIB, FcRL5, FcRn, and TRIM21. All FcγRs bind IgG at the cell surface, except FcRn and TRIM21 that bind IgG once internalized. The affinity of FcγRs for IgG is determined by polymorphisms of human FcγRs and ranges from 2 × 10(4) to 8 × 10(7) M(−1). The biological functions of FcγRs extend from cellular activation or inhibition, IgG-internalization/endocytosis/phagocytosis to IgG transport and recycling. This review focuses on human FcγRs and intends to present an overview of the current understanding of how these receptors may contribute to various pathologies. It will define FcγRs and their polymorphic variants, their affinity for human IgG subclasses, and review the associations found between FcγR polymorphisms and human pathologies. It will also describe the human FcγR-transgenic mice that have been used to study the role of these receptors in autoimmune, inflammatory, and allergic disease models. Frontiers Media S.A. 2014-05-30 /pmc/articles/PMC4038777/ /pubmed/24910634 http://dx.doi.org/10.3389/fimmu.2014.00254 Text en Copyright © 2014 Gillis, Gouel-Chéron, Jönsson and Bruhns. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Gillis, Caitlin
Gouel-Chéron, Aurélie
Jönsson, Friederike
Bruhns, Pierre
Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies
title Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies
title_full Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies
title_fullStr Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies
title_full_unstemmed Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies
title_short Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies
title_sort contribution of human fcγrs to disease with evidence from human polymorphisms and transgenic animal studies
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038777/
https://www.ncbi.nlm.nih.gov/pubmed/24910634
http://dx.doi.org/10.3389/fimmu.2014.00254
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