Abstract
CD4+ T cells turn pathological during heart failure (HF). We show that the expression of tumor necrosis factor (TNF)-α and tumor necrosis factor receptor (TNFR1) increases in HF-activated CD4+ T cells. However, the role of the TNF-α/TNFR1 axis in T-cell activation/proliferation is unknown. We show that TNFR1 neutralization during T-cell activation (ex vivo) or the loss of TNFR1 in adoptively transferred HF-activated CD4+ T cells (in vivo) augments their prosurvival and proliferative signaling. Importantly, TNFR1 neutralization does not affect CD69 expression or the pathological activity of HF-activated TNFR1−/− CD4+ T cells. These results show that during HF TNFR1 plays an important role in quelling prosurvival and proliferative signals in CD4+ T cells without altering their pathological activity.
Original language | English |
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Pages (from-to) | 1038-1049 |
Number of pages | 12 |
Journal | JACC: Basic to Translational Science |
Volume | 7 |
Issue number | 10 |
DOIs | |
State | Published - Oct 2022 |
Keywords
- T lymphocytes
- heart failure
- left ventricular remodeling
- myocardial infarction
- tumor necrosis factor receptors