ReviewThe Biochemical journal2012
PI3K signalling in B- and T-lymphocytes: new developments and therapeutic advances.
Review in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
112 citing papers in PubMed, 215 citations in OpenAlex.
- Trial
- FPR2/ALX stimulation modulates microglia and natural killer cells to restrict autoimmune astrocytopathy.Acta pharmacologica Sinica · 2026Article
- Effect of PI3K-p110α Inhibitor Alpelisib in the Differentiation and Effector Functions of M-CSF and GM-CSF Macrophages.International journal of molecular sciences · 2026Article
- Emerging Therapeutic Strategies in Cutaneous T-Cell Lymphoma: A Comprehensive Review of Clinical Trials.American journal of clinical dermatology · 2026Review
- Targeting FN1 to overcome gemcitabine resistance in gallbladder cancer: Mechanistic insights and an iRGD-modified PEG-PLGA nanoparticle delivery strategy.Materials today. Bio · 2026Article
- Lymphoproliferation in Inborn Errors of Immunity: Mechanisms, Manifestations and Clinical Management, with a Focus on ALPID.ImmunoTargets and therapy · 2026Review
- Multi-omics integration analysis identifies INPP4B as a T-cell-specific activation suppressor.Clinical and translational medicine · 2025Article
- Hypothesis of a CD137/Eomes activating axis for effector T cells in HPV oropharyngeal cancers.Molecular medicine (Cambridge, Mass.) · 2024Article
- Dietary supplementation of nucleotides and oligosaccharides in kittens reduces the expression of circulating miR-1-3p, miR-133a-3p, miR-206-3p and miR-383-5p.Frontiers in veterinary science · 2024Article
- Protective effect of thymol on glycerol-induced acute kidney injury.Renal failure · 2023Article
- Phospholipase C-γ as a Potential Therapeutic Target for Graves' Orbitopathy.Endocrinology and metabolism (Seoul, Korea) · 2023Article
- Review
- Mitigating Serious Adverse Events in Gene Therapy with AAV Vectors: Vector Dose and Immunosuppression.Drugs · 2023Review
- Can Soluble Immune Checkpoint Molecules on Exosomes Mediate Inflammation?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Review
- The Novel IGF-1R Inhibitor PB-020 Acts Synergistically with Anti-PD-1 and Mebendazole against Colorectal Cancer.Cancers · 2022Article
- Review
- Review
- Apolipoprotein A1 Modulates Teff/Treg Balance Through Scavenger Receptor Class B Type I-Dependent Mechanisms in Experimental Autoimmune Uveitis.Investigative ophthalmology & visual science · 2022Article
- Extranodal Natural Killer/T-Cell Lymphomas: Current Approaches and Future Directions.Journal of clinical medicine · 2022Review
- Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activation of PI3K (phosphoinositide 3-kinase) is a shared response to engagement of diverse types of transmembrane receptors. Depending on the cell type and stimulus, PI3K activation can promote different fates including proliferation, survival, migration and differentiation. The diverse roles of PI3K signalling are well illustrated by studies of lymphocytes, the cells that mediate adaptive immunity. Genetic and pharmacological experiments have shown that PI3K activation regulates many steps in the development, activation and differentiation of both B- and T-cells. These findings have prompted the development of PI3K inhibitors for the treatment of autoimmunity and inflammatory diseases. PI3K activation, however, has both positive and negative roles in immune system activation. Consequently, although PI3K suppression can attenuate immune responses it can also enhance inflammation, disrupt peripheral tolerance and promote autoimmunity. An exciting discovery is that a selective inhibitor of the p110δ catalytic isoform of PI3K, CAL-101, achieves impressive clinical efficacy in certain B-cell malignancies. A model is emerging in which p110δ inhibition disrupts signals from the lymphoid microenvironment, leading to release of leukaemia and lymphoma cells from their protective niche. These encouraging findings have given further momentum to PI3K drug development efforts in both cancer and immune diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.