# The NF-κB RelA transcription factor is not required for CD8+ T-cell function in acute viral infection and cancer

## TL;DR

This study shows that the RelA protein is not essential for CD8+ T cells to fight viruses or cancer.

## Contribution

A novel mouse model and gene-edited human cells reveal RelA is not required for CD8+ T-cell function in vivo.

## Key findings

- RelA ablation altered the transcriptome of CD8+ T cells but did not impair their proliferation.
- RelA deficiency had no impact on CD8+ T-cell responses to viral infection or tumors in vivo.
- CD8+ T cells can maintain protective functions without RelA in pathological contexts.

## Abstract

CD8+ T cells are critical mediators of pathogen clearance and anti-tumor immunity. Although signaling pathways leading to the activation of NF-κB transcription factors have crucial functions in the regulation of immune responses, the CD8+ T cell-autonomous roles of the different NF-κB subunits, are still unresolved. Here, we investigated the function of the ubiquitously expressed transcription factor RelA in CD8+ T-cell biology using a novel mouse model and gene-edited human cells. We found that CD8+ T cell-specific ablation of RelA markedly altered the transcriptome of ex vivo stimulated cells, but maintained the proliferative capacity of both mouse and human cells. In contrast, in vivo experiments showed that RelA deficiency did not affect the CD8+ T-cell response to acute viral infection or transplanted tumors. Our data suggest that in CD8+ T cells, RelA is dispensable for their protective activity in pathological contexts.