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The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway
INTRODUCTION: Atrial fibrillation (AF) represents the most common cardiac arrhythmia in daily clinical practice and substantially impacts affected patients by elevation of both morbidity and mortality. Previous investigations proved that inflammatory processes are closely linked to this multifactori...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8572810/ https://www.ncbi.nlm.nih.gov/pubmed/34536081 http://dx.doi.org/10.1007/s00011-021-01502-w |
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author | Hammer, Andreas Niessner, Alexander Sulzgruber, Patrick |
author_facet | Hammer, Andreas Niessner, Alexander Sulzgruber, Patrick |
author_sort | Hammer, Andreas |
collection | PubMed |
description | INTRODUCTION: Atrial fibrillation (AF) represents the most common cardiac arrhythmia in daily clinical practice and substantially impacts affected patients by elevation of both morbidity and mortality. Previous investigations proved that inflammatory processes are closely linked to this multifactorial pathogenesis—especially autoreactive CD4(+)CD28(null) T cells received in-depth attention. PURPOSE: Consequently, a potential pathophysiological pathway of the impact of CD4(+)CD28null T lymphocytes on the development and progression AF can be outlined. CONCLUSION: Considering the available data in the literature, it needs to be assumed that CD4(+)CD28(null) T lymphocytes are mainly involved in the development of AF and disease progression. Of utmost importance, it can be considered as the result of a T-cell-mediated auto-immune reaction among myocardial tissue. However, mechanisms which recruit CD4(+)CD28(null) cells in cardiac tissue remain unclear and need further investigation. |
format | Online Article Text |
id | pubmed-8572810 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-85728102021-11-15 The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway Hammer, Andreas Niessner, Alexander Sulzgruber, Patrick Inflamm Res Commentary INTRODUCTION: Atrial fibrillation (AF) represents the most common cardiac arrhythmia in daily clinical practice and substantially impacts affected patients by elevation of both morbidity and mortality. Previous investigations proved that inflammatory processes are closely linked to this multifactorial pathogenesis—especially autoreactive CD4(+)CD28(null) T cells received in-depth attention. PURPOSE: Consequently, a potential pathophysiological pathway of the impact of CD4(+)CD28null T lymphocytes on the development and progression AF can be outlined. CONCLUSION: Considering the available data in the literature, it needs to be assumed that CD4(+)CD28(null) T lymphocytes are mainly involved in the development of AF and disease progression. Of utmost importance, it can be considered as the result of a T-cell-mediated auto-immune reaction among myocardial tissue. However, mechanisms which recruit CD4(+)CD28(null) cells in cardiac tissue remain unclear and need further investigation. Springer International Publishing 2021-09-18 2021 /pmc/articles/PMC8572810/ /pubmed/34536081 http://dx.doi.org/10.1007/s00011-021-01502-w Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Commentary Hammer, Andreas Niessner, Alexander Sulzgruber, Patrick The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
title | The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
title_full | The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
title_fullStr | The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
title_full_unstemmed | The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
title_short | The impact of CD4(+)CD28(null) T lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
title_sort | impact of cd4(+)cd28(null) t lymphocytes on atrial fibrillation: a potential pathophysiological pathway |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8572810/ https://www.ncbi.nlm.nih.gov/pubmed/34536081 http://dx.doi.org/10.1007/s00011-021-01502-w |
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