Phosphoinositide 3-kinase δ is a regulatory T-cell target in cancer immunotherapy.


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Article
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Abstract

Tumour infiltration by regulatory T (Treg) cells contributes to suppression of the anti-tumour immune response, which limits the efficacy of immune-mediated cancer therapies. The phosphoinositide 3-kinase (PI3K) pathway has key roles in mediating the function of many immune cell subsets, including Treg cells. Treg function is context-dependent and depends on input from different cell surface receptors, many of which can activate the PI3K pathway. In this review, we explore how PI3Kδ contributes to signalling through several major immune cell receptors, including the T-cell receptor and co-stimulatory receptors such as CD28 and ICOS, but is antagonized by the immune checkpoint receptors CTLA-4 and PD-1. Understanding how PI3Kδ inhibition affects Treg signalling events will help to inform how best to use PI3Kδ inhibitors in clinical cancer treatment.

Description
Keywords
T cell, regulatory T cell, signal transduction, tumour immunology, Animals, Antineoplastic Agents, Class Ib Phosphatidylinositol 3-Kinase, Humans, Immunotherapy, Lymphocytes, Tumor-Infiltrating, Molecular Targeted Therapy, Neoplasms, Phenotype, Protein Kinase Inhibitors, Signal Transduction, T-Lymphocytes, Regulatory, Tumor Escape, Tumor Microenvironment
Journal Title
Immunology
Conference Name
Journal ISSN
0019-2805
1365-2567
Volume Title
157
Publisher
Wiley
Rights
All rights reserved