Repository logo
 

Inactivation of PI(3)K p110δ breaks regulatory T-cell-mediated immune tolerance to cancer.

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

Ali, Khaled 
Soond, Dalya R 
Pineiro, Roberto 
Hagemann, Thorsten 
Pearce, Wayne 

Abstract

Inhibitors against the p110δ isoform of phosphoinositide-3-OH kinase (PI(3)K) have shown remarkable therapeutic efficacy in some human leukaemias. As p110δ is primarily expressed in leukocytes, drugs against p110δ have not been considered for the treatment of solid tumours. Here we report that p110δ inactivation in mice protects against a broad range of cancers, including non-haematological solid tumours. We demonstrate that p110δ inactivation in regulatory T cells unleashes CD8(+) cytotoxic T cells and induces tumour regression. Thus, p110δ inhibitors can break tumour-induced immune tolerance and should be considered for wider use in oncology.

Description

Keywords

Animals, Antineoplastic Agents, Enzyme Activation, Enzyme Inhibitors, Immune Tolerance, Mice, Neoplasms, Phosphatidylinositol 3-Kinases, T-Lymphocytes, Regulatory

Journal Title

Nature

Conference Name

Journal ISSN

0028-0836
1476-4687

Volume Title

510

Publisher

Springer Science and Business Media LLC