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Phosphatidylinositol 3-Kinase p110δ Isoform Regulates CD8+ T Cell Responses during Acute Viral and Intracellular Bacterial Infections
Journal article   Open access   Peer reviewed

Phosphatidylinositol 3-Kinase p110δ Isoform Regulates CD8+ T Cell Responses during Acute Viral and Intracellular Bacterial Infections

Donald T Gracias, Alina C Boesteanu, Joseph A Fraietta, Jennifer L Hope, Alison J Carey, Yvonne M Mueller, Omkar U Kawalekar, Adam J Fike, Carl H June and Peter D Katsikis
The Journal of immunology (1950), v 196(3), pp 1186-1198
01 Feb 2016
PMID: 26740110
url
https://doi.org/10.4049/jimmunol.1501890View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

Adoptive Transfer Animals Bacterial Infections - enzymology Bacterial Infections - immunology CD8-Positive T-Lymphocytes - enzymology CD8-Positive T-Lymphocytes - immunology Female Flow Cytometry Immunologic Memory - immunology Isoenzymes - immunology Lymphocyte Activation - immunology Mice Mice, Knockout Phosphatidylinositol 3-Kinases - immunology Signal Transduction - immunology Virus Diseases - enzymology Virus Diseases - immunology
The p110δ isoform of PI3K is known to play an important role in immunity, yet its contribution to CTL responses has not been fully elucidated. Using murine p110δ-deficient CD8(+) T cells, we demonstrated a critical role for the p110δ subunit in the generation of optimal primary and memory CD8(+) T cell responses. This was demonstrated in both acute viral and intracellular bacterial infections in mice. We show that p110δ signaling is required for CD8(+) T cell activation, proliferation and effector cytokine production. We provide evidence that the effects of p110δ signaling are mediated via Akt activation and through the regulation of TCR-activated oxidative phosphorylation and aerobic glycolysis. In light of recent clinical trials that employ drugs targeting p110δ in certain cancers and other diseases, our study suggests caution in using these drugs in patients, as they could potentially increase susceptibility to infectious diseases. These studies therefore reveal a novel and direct role for p110δ signaling in in vivo CD8(+) T cell immunity to microbial pathogens.

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Web of Science research areas
Immunology
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