ArticleBMC musculoskeletal disorders2010
Loss of phosphoinositide 3-kinase gamma decreases migration and activation of phagocytes but not T cell activation in antigen-induced arthritis.
Article in BMC musculoskeletal disorders, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Phosphoinositide Signaling in Immune Cell Migration.Biomolecules · 2023Review
- Article
- Article
- Canonical PI3Kγ signaling in myeloid cells restricts Trypanosoma cruzi infection and dampens chagasic myocarditis.Nature communications · 2018Article
- Targeting PI3Kγ activity decreases vascular trauma-induced intimal hyperplasia through modulation of the Th1 response.The Journal of experimental medicine · 2014Article
- PI3Kγ kinase activity is required for optimal T-cell activation and differentiation.European journal of immunology · 2013Article
- PI3Kγ drives priming and survival of autoreactive CD4(+) T cells during experimental autoimmune encephalomyelitis.PloS one · 2012Article
- The Role of the PI3K Signaling Pathway in CD4(+) T Cell Differentiation and Function.Frontiers in immunology · 2012Article
- Potent anti-inflammatory and antinociceptive activity of the endothelin receptor antagonist bosentan in monoarthritic mice.Arthritis research & therapy · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPhosphoinositide 3-kinase gamma (PI3Kgamma) has been depicted as a major regulator of inflammatory processes, including leukocyte activation and migration towards several chemokines. This study aims to explore the role of PI3Kgamma in the murine model of antigen-induced arthritis (AIA).
methodsDevelopment of AIA was investigated in wildtype and PI3Kgamma-deficient mice as well as in mice treated with a specific inhibitor of PI3Kgamma (AS-605240) in comparison to untreated animals. Inflammatory reactions of leukocytes, including macrophage and T cell activation, and macrophage migration, were studied in vivo and in vitro.
resultsGenetic deletion or pharmacological inhibition of PI3Kgamma induced a marked decrease of clinical symptoms in early AIA, together with a considerably diminished macrophage migration and activation (lower production of NO, IL-1beta, IL-6). Also, macrophage and neutrophil infiltration into the knee joint were impaired in vivo. However, T cell functions, measured by cytokine production (TNFalpha, IFNgamma, IL-2, IL-4, IL-5, IL-17) in vitro and DTH reaction in vivo were not altered, and accordingly, disease developed normally at later timepoints
conclusionPI3Kgamma specifically affects phagocyte function in the AIA model but has no impact on T cell activation.
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