TNFR1 neutralization or loss in heart failure-activated CD4+ T cells augments their prosurvival and proliferative signaling without altering their pathological activity.
During heart failure, TNFR1 plays a role in quelling prosurvival and proliferative signals in pathological CD4+ T cells without altering their pathological activity.
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.
Kumar et al. (Wed,) conducted a other in Heart failure. TNFR1 neutralization or loss was evaluated on Prosurvival and proliferative signaling in CD4+ T cells. TNFR1 neutralization or loss in heart failure-activated CD4+ T cells augments their prosurvival and proliferative signaling without altering their pathological activity.