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Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB

Monoclonal antibodies (mAb) are revolutionising the treatment of many different diseases. Given their differing mode of action compared to most conventional chemotherapeutics and small molecule inhibitors, they possess the potential to be independent of common modes of treatment resistance and can t...

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Detalles Bibliográficos
Autores principales: Stopforth, Richard J., Cleary, Kirstie L. S., Cragg, Mark S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4891381/
https://www.ncbi.nlm.nih.gov/pubmed/26922075
http://dx.doi.org/10.1007/s10875-016-0247-8
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author Stopforth, Richard J.
Cleary, Kirstie L. S.
Cragg, Mark S.
author_facet Stopforth, Richard J.
Cleary, Kirstie L. S.
Cragg, Mark S.
author_sort Stopforth, Richard J.
collection PubMed
description Monoclonal antibodies (mAb) are revolutionising the treatment of many different diseases. Given their differing mode of action compared to most conventional chemotherapeutics and small molecule inhibitors, they possess the potential to be independent of common modes of treatment resistance and can typically be combined readily with existing treatments without dose-limiting toxicity. However, treatments with mAb rarely result in cure and so a full understanding of how these reagents work and can be optimised is key for their subsequent improvement. Here we review how an understanding of the biology of the inhibitory Fc receptor, FcγRIIB (CD32B), is leading to the development of improved mAb treatments.
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spelling pubmed-48913812016-06-17 Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB Stopforth, Richard J. Cleary, Kirstie L. S. Cragg, Mark S. J Clin Immunol Article Monoclonal antibodies (mAb) are revolutionising the treatment of many different diseases. Given their differing mode of action compared to most conventional chemotherapeutics and small molecule inhibitors, they possess the potential to be independent of common modes of treatment resistance and can typically be combined readily with existing treatments without dose-limiting toxicity. However, treatments with mAb rarely result in cure and so a full understanding of how these reagents work and can be optimised is key for their subsequent improvement. Here we review how an understanding of the biology of the inhibitory Fc receptor, FcγRIIB (CD32B), is leading to the development of improved mAb treatments. Springer US 2016-02-27 2016 /pmc/articles/PMC4891381/ /pubmed/26922075 http://dx.doi.org/10.1007/s10875-016-0247-8 Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Article
Stopforth, Richard J.
Cleary, Kirstie L. S.
Cragg, Mark S.
Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB
title Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB
title_full Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB
title_fullStr Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB
title_full_unstemmed Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB
title_short Regulation of Monoclonal Antibody Immunotherapy by FcγRIIB
title_sort regulation of monoclonal antibody immunotherapy by fcγriib
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4891381/
https://www.ncbi.nlm.nih.gov/pubmed/26922075
http://dx.doi.org/10.1007/s10875-016-0247-8
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