Authors: SARITA NEHRA, Rachel Rosenzweig, Oscar Bermeo-Blanco, ERIC X BECK, Noah L Weisleder, Richard J Gumina, Shyam S Bansal
Published: 2020-10-27
DOI: 10.1161/res.127.suppl_1.429
Source: Full article
Ischemic heart failure (HF) results in the activation of self-reactive CD4+ T-lymphocytes against unknown cardiac antigens. The mechanisms that mediate the survival of self-reactive T-cells during ischemic HF are not known. TNF mediated NF-kB signaling regulates cellular apoptotic pathways and T cells express high levels of TNF receptor-1 (TNFR1) during chronic heart failure. Thus, we hypothesized that TNFR1 regulates pro-apoptotic signaling through NF-kB and is critical for the clearance of self-reactive T-cells during HF. To test this, male WT or TNFR1