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Updated: Aug 25, 2025

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol
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In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

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PI3K Isoforms in CD8+ T Cell Development and Function

Pankaj Gaur1, Mikayel Mkrtichyan1, Vivek Verma1

  • 1The Loop Immuno-Oncology Laboratory, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.

Current Topics in Microbiology and Immunology
|October 15, 2022
PubMed

CD8+ T cells are an essential part of the immune system and play a vital role in defending against tumors and infections. The phosphoinositide-3-kinase (PI3K), especially class I, is involved in numerous interrelated signaling pathways which control CD8+ T cell development, maturation, migration, activation, and differentiation. While CD8+ T lymphocytes express all class I PI3K isoforms (PI3Kα, PI3Kβ, PI3Kδ, and PI3Kγ), isoform-specific functions, especially for PI3Kα and PI3Kβ have not been fully elucidated. A few studies suggest the important role of p110δ and p110γ in CD8+ T cell activation, signaling, chemotaxis and function and several clinical trials are currently testing the effect of isoform-specific inhibitors in various types of cancers, including Indolent Non-Hodgkin Lymphoma, Peripheral T cell Lymphoma, Chronic Lymphocytic Leukemia, Small Lymphocytic Lymphoma, non-small cell lung carcinoma (NSCLC), head & neck cancer, and breast cancer. This chapter summarizes current knowledge of the roles of various PI3K isoforms and downstream signaling pathways in regulating CD8+ T cell fate, including cell proliferation, migration, and memory generation. We also discuss certain clinical trials employing PI3K inhibitors for cancer therapy, their limitations, and future perspectives.

Keywords:
CD8+ T cellMemoryMigrationPI3K signalingPI3KγPI3KδSurvival

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