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 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.

Automated summary

Inflammatory processes and autoreactive CD4(+)CD28(null) T cells are closely linked to the development and progression of atrial fibrillation (AF), potentially leading to T-cell-mediated autoimmune reactions in myocardial tissue. However, mechanisms recruiting CD4(+)CD28(null) cells in cardiac tissue remain unclear and require further investigation.