論文

2021年6月18日

Phosphoinositide 3-Kinase p110 Delta Differentially Restrains and Directs Naïve Versus Effector CD8+ T Cell Transcriptional Programs.

Frontiers in immunology
  • Aneela Nomura

記述言語
掲載種別
研究論文(学術雑誌)
DOI
10.3389/fimmu.2021.691997

Phosphoinositide 3-kinase p110 delta (PI3K p110δ) is pivotal for CD8+ T cell immune responses. The current study explores PI3K p110δ induction and repression of antigen receptor and cytokine regulated programs to inform how PI3K p110δ directs CD8+ T cell fate. The studies force a revision of the concept that PI3K p110δ controls metabolic pathways in T cells and reveal major differences in PI3K p110δ regulated transcriptional programs between naïve and effector cytotoxic T cells (CTL). These differences include differential control of the expression of cytolytic effector molecules and costimulatory receptors. Key insights from the work include that PI3K p110δ signalling pathways repress expression of the critical inhibitory receptors CTLA4 and SLAMF6 in CTL. Moreover, in both naïve and effector T cells the dominant role for PI3K p110δ is to restrain the production of the chemokines that orchestrate communication between adaptive and innate immune cells. The study provides a comprehensive resource for understanding how PI3K p110δ uses multiple processes mediated by Protein Kinase B/AKT, FOXO1 dependent and independent mechanisms and mitogen-activated protein kinases (MAPK) to direct CD8+ T cell fate.

リンク情報
DOI
https://doi.org/10.3389/fimmu.2021.691997
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/34220851
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8250422
URL
https://europepmc.org/articles/PMC8250422
ID情報
  • DOI : 10.3389/fimmu.2021.691997
  • ORCIDのPut Code : 120135276
  • PubMed ID : 34220851
  • PubMed Central 記事ID : PMC8250422

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