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

Nature. 2014 Jun 19;510(7505):407-411. doi: 10.1038/nature13444. Epub 2014 Jun 11.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology*
  • Immune Tolerance / drug effects*
  • Immune Tolerance / immunology
  • Mice
  • Neoplasms / enzymology*
  • Neoplasms / immunology*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • T-Lymphocytes, Regulatory / drug effects*
  • T-Lymphocytes, Regulatory / enzymology
  • T-Lymphocytes, Regulatory / immunology

Substances

  • Antineoplastic Agents
  • Enzyme Inhibitors
  • Phosphatidylinositol 3-Kinases