IFNγ Helps CBLB-Deficient CD8+ T Cells to Put Up Resistance to Tregs

In this issue, Han and colleagues demonstrate in preclinical cancer models that genetic deletion of the E3 ubiquitin ligase Cbl proto-oncogene B (CBLB) in adoptively transferred CD8(+) T cells induces resistance to regulatory T cells. CBLB deletion induces IFN gamma and downmodulates TGF beta/SMAD signaling. This ultimately enforces these cells to be way more effective against various cancers.

Automated summary

In preclinical cancer models, the genetic deletion of CBLB gene enhances the resistance of adoptively transferred CD8(+) T cells to regulatory T cells, resulting in a higher efficacy against various cancers.