Concomitant deletion of Ptpn6 and Ptpn11 in T cells fails to improve anticancer responses

ABSTRACT: Anticancer T cells acquire a dysfunctional state characterized by poor effector function and expression of inhibitory receptors, such as PD-1. Blockade of PD-1 leads to T cell reinvigoration and is increasingly applied as an effective anticancer treatment. Recent work challenged the commonly held view that the phosphatase PTPN11 (known as SHP-2) is essential for PD-1 signalling in T cells, suggesting functional redundancy with the homologous phosphatase PTPN6 (SHP-1). Therefore, we investigated the effect of concomitant Ptpn6 and Ptpn11 deletion in T cells on their ability to mount antitumour responses. In vivo data shows that neither sustained nor acute Ptpn6/11 deletion improves T cell-mediated tumour control. Sustained loss of Ptpn6/11 also impairs the therapeutic effects of anti-PD1 t

SUBMITTER: Pedro Ventura 

PROVIDER: S-SCDT-EMBOR-2022-55399V1 | biostudies-other |

REPOSITORIES: biostudies-other