ArticlePloS one2012
Genetic or pharmaceutical blockade of phosphoinositide 3-kinase p110δ prevents chronic rejection of heart allografts.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- PI3K in T Cell Adhesion and Trafficking.Frontiers in immunology · 2021Review
- Targeting the class IA PI3K isoforms p110α/δ attenuates heart allograft rejection in mice by suppressing the CD4American journal of translational research · 2018Article
- Obesity-Induced Metabolic Stress Leads to Biased Effector Memory CD4Cell metabolism · 2017Article
- Mechanisms of T cell organotropism.Cellular and molecular life sciences : CMLS · 2016Review
- Δ⁹-Tetrahydrocannabinol attenuates allogeneic host-versus-graft response and delays skin graft rejection through activation of cannabinoid receptor 1 and induction of myeloid-derived suppressor cells.Journal of leukocyte biology · 2015Article
- PI3K inhibitors in inflammation, autoimmunity and cancer.Current opinion in pharmacology · 2015Review
- Innate PI3K p110δ regulates Th1/Th17 development and microbiota-dependent colitis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- An analysis of the global expression of microRNAs in an experimental model of physiological left ventricular hypertrophy.PloS one · 2014Article
- Targeting PI3Kδ: One man's meat is another man's poison.Oncoimmunology · 2013Article
- T cell trafficking and metabolism: novel mechanisms and targets for immunomodulation.Current opinion in pharmacology · 2012Review
- All PI3Kinase signaling is not mTOR: dissecting mTOR-dependent and independent signaling pathways in T cells.Frontiers in immunology · 2012Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Chronic rejection is the major cause of long-term heart allograft failure, characterized by tissue infiltration by recipient T cells with indirect allospecificity. Phosphoinositol-3-kinase p110δ is a key mediator of T cell receptor signaling, regulating both T cell activation and migration of primed T cells to non-lymphoid antigen-rich tissue. We investigated the effect of genetic or pharmacologic inactivation of PI3K p110δ on the development of chronic allograft rejection in a murine model in which HY-mismatched male hearts were transplanted into female recipients. We show that suppression of p110δ activity significantly attenuates the development of chronic rejection of heart grafts in the absence of any additional immunosuppressive treatment by impairing the localization of antigen-specific T cells to the grafts, while not inducing specific T cell tolerance. p110δ pharmacologic inactivation is effective when initiated after transplantation. Targeting p110δ activity might be a viable strategy for the treatment of heart chronic rejection in humans.
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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.