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Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes

Autoimmune diseases are often associated with autoantibodies that abnormally target self-antigens (autoantigens). An intuitive therapeutic strategy for diseases caused by aAbs is to design decoys, or soluble molecules that target the antigen combining site of these aAbs, thereby blocking binding of...

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Autores principales: Cardozo, Timothy, Cardozo, Lila, Boutjdir, Mohamed
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8832015/
https://www.ncbi.nlm.nih.gov/pubmed/35154130
http://dx.doi.org/10.3389/fimmu.2022.812649
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author Cardozo, Timothy
Cardozo, Lila
Boutjdir, Mohamed
author_facet Cardozo, Timothy
Cardozo, Lila
Boutjdir, Mohamed
author_sort Cardozo, Timothy
collection PubMed
description Autoimmune diseases are often associated with autoantibodies that abnormally target self-antigens (autoantigens). An intuitive therapeutic strategy for diseases caused by aAbs is to design decoys, or soluble molecules that target the antigen combining site of these aAbs, thereby blocking binding of aAb to self-antigen and subsequent tissue damage. Here, we review the known decoy molecules of these types, discuss newer technological opportunities afforded by monoclonal antibody and structural biology advances, and discuss the challenges to this approach. Recent opportunities relevant to this approach for cardiac phenotypes, specifically Ro-associated long QT syndrome, are discussed.
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spelling pubmed-88320152022-02-12 Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes Cardozo, Timothy Cardozo, Lila Boutjdir, Mohamed Front Immunol Immunology Autoimmune diseases are often associated with autoantibodies that abnormally target self-antigens (autoantigens). An intuitive therapeutic strategy for diseases caused by aAbs is to design decoys, or soluble molecules that target the antigen combining site of these aAbs, thereby blocking binding of aAb to self-antigen and subsequent tissue damage. Here, we review the known decoy molecules of these types, discuss newer technological opportunities afforded by monoclonal antibody and structural biology advances, and discuss the challenges to this approach. Recent opportunities relevant to this approach for cardiac phenotypes, specifically Ro-associated long QT syndrome, are discussed. Frontiers Media S.A. 2022-01-28 /pmc/articles/PMC8832015/ /pubmed/35154130 http://dx.doi.org/10.3389/fimmu.2022.812649 Text en Copyright © 2022 Cardozo, Cardozo and Boutjdir https://creativecommons.org/licenses/by/4.0/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) and the copyright owner(s) 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
Cardozo, Timothy
Cardozo, Lila
Boutjdir, Mohamed
Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes
title Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes
title_full Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes
title_fullStr Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes
title_full_unstemmed Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes
title_short Autoantibody:Autoantigen Competitor Decoys: Application to Cardiac Phenotypes
title_sort autoantibody:autoantigen competitor decoys: application to cardiac phenotypes
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8832015/
https://www.ncbi.nlm.nih.gov/pubmed/35154130
http://dx.doi.org/10.3389/fimmu.2022.812649
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