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Phosphoinositide 3‐kinase δ is a regulatory T‐cell target in cancer immunotherapy
Author(s) -
Lim Ee Lyn,
Okkenhaug Klaus
Publication year - 2019
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13082
Subject(s) - immune system , receptor , cancer research , cancer immunotherapy , biology , immunotherapy , immune receptor , signal transduction , t cell , microbiology and biotechnology , context (archaeology) , immunology , biochemistry , paleontology
Summary 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 ( PI 3K) 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 PI 3K pathway. In this review, we explore how PI 3K δ contributes to signalling through several major immune cell receptors, including the T‐cell receptor and co‐stimulatory receptors such as CD 28 and ICOS , but is antagonized by the immune checkpoint receptors CTLA ‐4 and PD ‐1. Understanding how PI 3K δ inhibition affects Treg signalling events will help to inform how best to use PI 3K δ inhibitors in clinical cancer treatment.