ArticleThe Journal of clinical investigation2008
T cell receptor-induced phosphoinositide-3-kinase p110delta activity is required for T cell localization to antigenic tissue in mice.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Phosphoinositide Signaling in Immune Cell Migration.Biomolecules · 2023Review
- PI3K Isoforms in CD8Current topics in microbiology and immunology · 2022Article
- Hyperactive PI3Kδ predisposes naive T cells to activation via aerobic glycolysis programs.Cellular & molecular immunology · 2021Article
- Non-neuronal cells in amyotrophic lateral sclerosis - from pathogenesis to biomarkers.Nature reviews. Neurology · 2021Review
- PI3K in T Cell Adhesion and Trafficking.Frontiers in immunology · 2021Review
- Dynamic Regulation of the Molecular Mechanisms of Regulatory T Cell Migration in Inflamed Skin.Frontiers in immunology · 2021Article
- Defining Bronchial Asthma with Phosphoinositide 3-Kinase Delta Activation: Towards Endotype-Driven Management.International journal of molecular sciences · 2019Review
- Comparison of interleukin-2-inducible kinase (ITK) inhibitors and potential for combination therapies for T-cell lymphoma.Scientific reports · 2018Article
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- Phosphoinositide 3-Kinase in Asthma: Novel Roles and Therapeutic Approaches.American journal of respiratory cell and molecular biology · 2017Review
- Anti-inflammatory potential of PI3Kδ and JAK inhibitors in asthma patients.Respiratory research · 2016Article
- Mechanisms of T cell organotropism.Cellular and molecular life sciences : CMLS · 2016Review
- PI3Kδ promotes CD4(+) T-cell interactions with antigen-presenting cells by increasing LFA-1 binding to ICAM-1.Immunology and cell biology · 2016Article
- CD31 signals confer immune privilege to the vascular endothelium.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Lactate Regulates Metabolic and Pro-inflammatory Circuits in Control of T Cell Migration and Effector Functions.PLoS biology · 2015Article
- Self-recognition of the endothelium enables regulatory T-cell trafficking and defines the kinetics of immune regulation.Nature communications · 2014Article
- CD31 exhibits multiple roles in regulating T lymphocyte trafficking in vivo.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Molecular mechanisms of metabolic reprogramming in proliferating cells: implications for T-cell-mediated immunity.Immunology · 2012Review
- T cell trafficking and metabolism: novel mechanisms and targets for immunomodulation.Current opinion in pharmacology · 2012Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
The establishment of T cell-mediated inflammation requires the migration of primed T lymphocytes from the blood stream and their retention in antigenic sites. While naive T lymphocyte recirculation in the lymph and blood is constitutively regulated and occurs in the absence of inflammation, the recruitment of primed T cells to nonlymphoid tissue and their retention at the site are enhanced by various inflammatory signals, including TCR engagement by antigen-displaying endothelium and resident antigen-presenting cells. In this study, we investigated whether signals downstream of TCR ligation mediated by the phosphoinositide-3-kinase (PI3K) subunit p110delta contributed to the regulation of these events. T lymphocytes from mice expressing catalytically inactive p110delta displayed normal constitutive trafficking and migratory responses to nonspecific stimuli. However, these cells lost susceptibility to TCR-induced migration and failed to localize efficiently to antigenic tissue. Importantly, we showed that antigen-induced T cell trafficking and subsequent inflammation was abrogated by selective pharmacological inhibition of PI3K p110delta activity. These observations suggest that pharmacological targeting of p110delta activity is a viable strategy for the therapy of T cell-mediated pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.