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the lack of PI3Kgamma favors M1 macrophages polarization providing an inflammatory-prone environment, which does not prevent kidney diseases progression.
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Deficient mice in the canonical PI3Kgamma signaling (Pik3cg-/-) are more susceptible to T. cruzi infection. The canonical PI3Kgamma signaling in myeloid cells restricts heart parasitism and avoids heart damage and death of mice.
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the beneficial action of PI3Kgamma ablation in obesity-driven glucose intolerance is largely a result of its leptin-dependent effects on adiposity and, to a lesser extent, the promotion of adipose tissue neutrophil recruitment and M1 polarization of gene expression
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As blockade of PI3Kgamma or integrin alpha4 prevents accumulation of myeloid-derived suppressor cells and reduces myeloid cell expression of immunosuppressive factors that stimulate tumor immune escape, these results highlight PI3Kgamma and integrin alpha4 as targets for the design of cancer therapeutics.
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PI3K( PI3Kgamma(null) versus PI3Kgamma(WT) mice) inhibition slows tumor growth, enhances antitumor immunity, and heightens susceptibility to immune checkpoint inhibitors. We propose that combining PI3K inhibition with anti-PD1 may be a viable therapeutic approach for triple-negative breast cancer
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PI3Kg ablation protects mice from obesity, inflammation, and insulin resistance caused by high-fat diet feeding.
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The results showed that PI3K-gamma is likely a crucial element in sepsis-induced myocardial dysfunction (SIMD) by regulating the PI3K/Akt pathway, and become a new marker of myocardial injury. Inhibition of PI3K-gamma might be a potential therapeutic target in SIMD.
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Phosphatidylinositol-3-kinases (PI3K) gamma and delta are key regulators of T cell signaling. Here the author show, using mouse heart allograft transplantation models, that PI3Kgamma or PI3Kdelta deficiency prolongs graft survival, but selective inhibition of PI3Kgamma or PI3Kdelta reveals alternative transplant survival outcomes post CTLA4-Ig treatment.
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PI3Kgamma kinase activity-independent control of cAMP phosphodiesterase as a crucial mediator of microglial cAMP regulation, MMP-9 expression, and phagocytic activity following focal brain ischemia/recirculation.
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We report here that PI3Kgamma regulates macrophage transcriptional programming, leading to T-cell suppression, desmoplasia, and metastasis in pancreas adenocarcinoma.
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a STOP mutation in the GM-CSFRalpha chain, leading to a complete and specific deficiency in GM-CSF signaling, is reported.
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increased levels of eosinophils and IgE in p110gamma/delta-/- mice do not abolish the protective effect of p110gamma/delta-deficiency against OVAlbumin-induced allergic airway inflammation.
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The Effector PI3Kgamma Is Required for Toll-like Receptors-induced Akt/mTOR Signaling and Regulation of Cytokine Responses.
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macrophage PI 3-kinase gamma controls a critical switch between immune stimulation and suppression during inflammation and cancer; therapeutic targeting of intracellular signalling pathways that regulate the switch between macrophage polarization states can control immune suppression in cancer and other disorders
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Accumulation of PtdIns(3,4,5)P3, but not PtdIns(3,4)P2,in neutrophils were dependent on PI3Kgamma activity.
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identify PI3Kgamma as a novel key host protective factor in influenza virus infection and shed light on an unappreciated layer of complexity concerning the role of PI3K signaling in this context
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Pik3cg(-/-) mice had persistent lung inflammation induced by sepsis and increased in vascular permeability. Restoration of p110gamma in pulmonary endothelial cellsrestored endothelial regeneration and normalized the defective vascular repair program.
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Results found that the absence of PI3Kgamma significantly delayed mortality and reduced clinical signs and histopathological brain changes associated with Plasmodium berghei infection.
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The authors demonstrate that the Attention Deficit Disorder with Hyperactivity phenotype depends on a dysregulation of CREB signaling exerted by a kinase-independent PI3Kgamma-PDE4D interaction in the noradrenergic neurons of the locus coeruleus.
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platelet PI3Kgamma contributes to platelet-mediated vascular inflammation and carotid intima-media thickening after flow severely reduced. Platelet PI3Kgamma may be a new target in the treatment of vascular diseases.
