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Distinct cell-specific control of autoimmunity and infection by FcγRIIb

FcγRIIb is an inhibitory Fc receptor expressed on B cells and myeloid cells. It is important in controlling responses to infection, and reduced expression or function predisposes to autoimmunity. To determine if increased expression of FcγRIIb can modulate these processes, we created transgenic mice...

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Autores principales: Brownlie, Rebecca J., Lawlor, Kate E., Niederer, Heather A., Cutler, Antony J., Xiang, Zou, Clatworthy, Menna R., Floto, R. Andres, Greaves, David R., Lyons, Paul A., Smith, Kenneth G.C.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292226/
https://www.ncbi.nlm.nih.gov/pubmed/18362174
http://dx.doi.org/10.1084/jem.20072565
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author Brownlie, Rebecca J.
Lawlor, Kate E.
Niederer, Heather A.
Cutler, Antony J.
Xiang, Zou
Clatworthy, Menna R.
Floto, R. Andres
Greaves, David R.
Lyons, Paul A.
Smith, Kenneth G.C.
author_facet Brownlie, Rebecca J.
Lawlor, Kate E.
Niederer, Heather A.
Cutler, Antony J.
Xiang, Zou
Clatworthy, Menna R.
Floto, R. Andres
Greaves, David R.
Lyons, Paul A.
Smith, Kenneth G.C.
author_sort Brownlie, Rebecca J.
collection PubMed
description FcγRIIb is an inhibitory Fc receptor expressed on B cells and myeloid cells. It is important in controlling responses to infection, and reduced expression or function predisposes to autoimmunity. To determine if increased expression of FcγRIIb can modulate these processes, we created transgenic mice overexpressing FcγRIIb on B cells or macrophages. Overexpression of FcγRIIb on B cells reduced the immunoglobulin G component of T-dependent immune responses, led to early resolution of collagen-induced arthritis (CIA), and reduced spontaneous systemic lupus erythematosus (SLE). In contrast, overexpression on macrophages had no effect on immune responses, CIA, or SLE but increased mortality after Streptococcus pneumoniae infection. These results help define the role of FcγRIIb in immune responses, demonstrate the contrasting roles played by FcγRIIb on B cells and macrophages in the control of infection and autoimmunity, and emphasize the therapeutic potential for modulation of FcγRIIb expression on B cells in inflammatory and autoimmune disease.
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spelling pubmed-22922262008-10-14 Distinct cell-specific control of autoimmunity and infection by FcγRIIb Brownlie, Rebecca J. Lawlor, Kate E. Niederer, Heather A. Cutler, Antony J. Xiang, Zou Clatworthy, Menna R. Floto, R. Andres Greaves, David R. Lyons, Paul A. Smith, Kenneth G.C. J Exp Med Articles FcγRIIb is an inhibitory Fc receptor expressed on B cells and myeloid cells. It is important in controlling responses to infection, and reduced expression or function predisposes to autoimmunity. To determine if increased expression of FcγRIIb can modulate these processes, we created transgenic mice overexpressing FcγRIIb on B cells or macrophages. Overexpression of FcγRIIb on B cells reduced the immunoglobulin G component of T-dependent immune responses, led to early resolution of collagen-induced arthritis (CIA), and reduced spontaneous systemic lupus erythematosus (SLE). In contrast, overexpression on macrophages had no effect on immune responses, CIA, or SLE but increased mortality after Streptococcus pneumoniae infection. These results help define the role of FcγRIIb in immune responses, demonstrate the contrasting roles played by FcγRIIb on B cells and macrophages in the control of infection and autoimmunity, and emphasize the therapeutic potential for modulation of FcγRIIb expression on B cells in inflammatory and autoimmune disease. The Rockefeller University Press 2008-04-14 /pmc/articles/PMC2292226/ /pubmed/18362174 http://dx.doi.org/10.1084/jem.20072565 Text en Copyright © 2008, 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 Articles
Brownlie, Rebecca J.
Lawlor, Kate E.
Niederer, Heather A.
Cutler, Antony J.
Xiang, Zou
Clatworthy, Menna R.
Floto, R. Andres
Greaves, David R.
Lyons, Paul A.
Smith, Kenneth G.C.
Distinct cell-specific control of autoimmunity and infection by FcγRIIb
title Distinct cell-specific control of autoimmunity and infection by FcγRIIb
title_full Distinct cell-specific control of autoimmunity and infection by FcγRIIb
title_fullStr Distinct cell-specific control of autoimmunity and infection by FcγRIIb
title_full_unstemmed Distinct cell-specific control of autoimmunity and infection by FcγRIIb
title_short Distinct cell-specific control of autoimmunity and infection by FcγRIIb
title_sort distinct cell-specific control of autoimmunity and infection by fcγriib
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292226/
https://www.ncbi.nlm.nih.gov/pubmed/18362174
http://dx.doi.org/10.1084/jem.20072565
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