Key result
TNFR1 loss boosts heart failure-activated CD4+ T-cell survival ~10-fold without altering cardiac dysfunction.
Why the study?
CD4+ T cells turn pathological during heart failure, but the role of the TNF-alpha/TNFR1 axis in T-cell activation and proliferation is unknown.
Does TNFR1 neutralization or genetic deletion alter the survival, proliferation, activation, and pathological cardiac remodeling activity of heart failure-activated CD4+ T cells in a murine model of ischemic heart failure?
Does TNFR1 neutralization or genetic deletion alter the survival, proliferation, activation, and pathological cardiac remodeling activity of heart failure-activated CD4+ T cells in a murine model of ischemic heart failure?
This preclinical study demonstrates that TNFR1 acts as a negative regulator of survival and proliferation in pathological CD4+ T cells during ischemic heart failure without altering their pathogenicity, suggesting that immunomodulation in heart failure may require simultaneous TNFR1 activation and TNFR2 inhibition.
Answers are grounded in this paper and cite their sources.
TNFR1 loss boosts T-cell survival without worsening remodeling in mice; leaves open dual TNFR targeting for future HF immunomodulation trials.
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.
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Kumar et al. (2022) studied Ischemic heart failure (post-myocardial infarction) (n=165). TNFR1 neutralization (anti-TNFR1 antibody ex vivo) or TNFR1 genetic deletion (TNFR1-/- in vivo) vs. Stimulated wild-type CD4+ T cells without anti-TNFR1 antibody (ex vivo) or adoptive transfer of wild-type or sham CD4+ T cells (in vivo) was evaluated on Survival, proliferation, and pathogenicity (cardiac dysfunction) of adoptively transferred HF-activated CD4+ T cells at 14 weeks (10- to 11-fold higher donor CD4+ T-cell levels in spleen with TNFR1 loss; no difference in cardiac dysfunction, p=<0.05). TNFR1 loss in heart failure-activated CD4+ T cells increased splenic T-cell survival 10- to 11-fold and Bcl-xL expression ~4-fold without altering T-cell activation or induced cardiac dysfunction.
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