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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., Competing Interests: This work was supported by the National Institutes of Health grants to Dr Bansal (R00 HL132123 and R01 HL153164). Funding sources did not influence any part of this work. The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2022 The Authors.)