Transient targeting of phosphoinositide 3-kinase acts as a roadblock in mast cells' route to allergy

Collmann, Emilie; Bohnacker, Thomas; Marone, Romina; Dawson, Janet; Rehberg, Markus; Stringer, Rowan; Krombach, Fritz; Burkhart, Christoph; Hirsch, Emilio; Hollingworth, Gregory J.; Thomas, Matthew; Wymann, Matthias P.

doi:10.1016/j.jaci.2013.03.008

Cited by 29 publications

(27 citation statements)

References 53 publications

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“…Consequently, the in vivo inhibition of p110d or PI3Kg strongly reduces the anaphylactic allergic response in mice. Moreover, PI3Kd and PI3Kg isoforms have also been implicated in migration and cytokine secretion in this cell type in vivo (Collmann et al, 2013;Doukas et al, 2009;Nashed et al, 2007). Altogether, these studies strongly support the idea that the functions of the PI3Kd and PI3Kg isoforms complement each other in mast cells and could be important in a therapeutic context.…”

Section: Pi3k In Mast Cellssupporting

confidence: 67%

“…maturation and differentiation(Oak et al, 2006) Th17 response(Boyle et al, 2014) Mast cell Granule and pro-inflammatory mediators secretion(Ali et al, 2004;Ali et al, 2008) Migration and cytokine secretion(Collmann et al, 2013;Doukas et al, 2009; Nashed et al, 2007) B cell Development and survival(Clayton et al, 2002;Jou et al, 2002;Okkenhaug et al, 2002) Antigen-dependant activation(Ramadani et al, 2010) SMC PDGF-induced proliferation (via non-catalytic role) (Vantler et alpeptide -induced monocyte migration (Gayral et al, 2014) Chemotactism (Hirsch et al, 2000) (Jones et al, 2003) and adhesion (Diaz-Munoz et al, 2013; Weiss-Haljiti et al, 2004) Arterial wall infiltration during atherosclerosis (Fougerat et al, 2012; Gayral et al, 2014) Foam cell formation via pinocytosis (Anzinger et al, 2012) T cellT cell activation(Sasaki et al, 2000) Th17 differentiation(Bergamini et al, 2012) Th1 cytokine secretion during arterial injury(Smirnova et al, 2014) Mast cellGranule release(Laffargue et al, 2002;Wymann et al, 2003) Migration and cytokine secretion(Collmann et al, 2013;Doukas et al, 2009;Nashed et al, 2007) B cell Maturation, survival (Beer-Hammer et al, 2010) SMC PDGF-induced migration (Fougerat et al, 2012; Yao et al, 2014) Endothelial cell…”

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confidence: 99%

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PI3K signaling in arterial diseases: Non redundant functions of the PI3K isoforms

Lupieri

Smirnova

Malet

et al. 2015

Advances in Biological Regulation

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Section: Pi3k In Mast Cellssupporting

confidence: 67%

mentioning

confidence: 99%

PI3K signaling in arterial diseases: Non redundant functions of the PI3K isoforms

Lupieri

Smirnova

Malet

et al. 2015

Advances in Biological Regulation

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“…PI3Kγ is also critically involved in an autocrine/paracrine mast cell migration towards antigen (Kitaura et al, 2005; Endo et al, 2009). In contrast to the results obtained previously (Kuehn et al, 2010; Ali et al, 2008), the most recent work (Collmann et al, 2013) ruled out the role of PI3Kδ in antigen-mediated mast cell chemotaxis. Using p110γ knockout mice, p110γ KR mice (expressing catalytically inactive subunit of p110γ), p110δ knockout mice, the p110δ-specific inhibitor IC87114 and a novel p110γ-specific inhibitor NVS-PI3-4, the authors showed that PI3Kγ alone is responsible for accumulation of mast cells in IgE-challenged skin, cytokine release, and mast cell/endothelial interaction and chemotaxis.…”

Section: Chemotaxiscontrasting

confidence: 79%

Signal transduction and chemotaxis in mast cells

Dráber

Hálová

Polakovičová

et al. 2016

European Journal of Pharmacology

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Mast cells play crucial roles in both innate and adaptive arms of the immune system. Along with basophils, mast cells are essential effector cells for allergic inflammation that causes asthma, allergic rhinitis, food allergy and atopic dermatitis. Mast cells are usually increased in inflammatory sites of allergy and, upon activation, release various chemical, lipid, peptide and protein mediators of allergic reactions. Since antigen/immunoglobulin E (IgE)-mediated activation of these cells is a central event to trigger allergic reactions, innumerable studies have been conducted on how these cells are activated through cross-linking of the high-affinity IgE receptor (FcεRI). Development of mature mast cells from their progenitor cells is under the influence of several growth factors, of which the stem cell factor (SCF) seems to be the most important. Therefore, how SCF induces mast cell development and activation via its receptor, KIT, has been studied extensively, including a cross-talk between KIT and FcεRI signaling pathways. Although our understanding of the signaling mechanisms of the FcεRI and KIT pathways is far from complete, pharmaceutical applications of the knowledge about these pathways are underway. This review will focus on recent progresses in FcεRI and KIT signaling and chemotaxis.

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“…Whether similar differential MCp maturity exists in allergic versus nonallergic subjects and could condition the development of atopic respiratory disorders in adulthood warrants further investigation. In IgE-challenged skin, functional phosphoinositide 3-kinase (PI3K) γ but not δ is critical to MCp accumulation, TNF release and transendothelial migration and anaphylaxis [11]. …”

Section: MC Plasticity In Development and Maturationmentioning

confidence: 99%

Mast cell plasticity and sphingosine-1-phosphate in immunity, inflammation and cancer

Oskeritzian¹

2015

Molecular Immunology

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Mast cells (MC) are found in all vascularized tissues at homeostasis and, until recently, were viewed only as effector cells of allergic reactions via degranulation, the canonical process through which MC release mediators, including histamine and pre-formed proteases and cytokines such as TNF. Cross-linking of IgE bound to surface high affinity receptors for IgE (FcεRI) by a specific antigen (Ag) triggers signaling events leading to degranulation. We and others have reported the concomitant production and export of an influential multifaceted sphingolipid mediator, sphingosine-1-phosphate (S1P) transported outside of MC by ATP-binding cassettes (ABC) transporters, i.e., independently of degranulation. Indeed, the MC horizon expanded by the discovery of their unique ability to selectively release mediators depending upon the stimulus and receptors involved. Aside from degranulation and transporter usage, MC are also endowed with piecemeal degranulation, a slower process during which mediator release occurs with minor morphological changes. The broad spectrum of pro- and anti-inflammatory bioactive substances MC produce and release, their amounts and delivery pace render these cells bona fide fine-tuners of the immune response. In this viewpoint article, MC developmental, phenotypic and functional plasticity, its modulation by microRNAs and its relevance to immunity, inflammation and cancer will be discussed.

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Transient targeting of phosphoinositide 3-kinase acts as a roadblock in mast cells' route to allergy

Cited by 29 publications

References 53 publications

PI3K signaling in arterial diseases: Non redundant functions of the PI3K isoforms

PI3K signaling in arterial diseases: Non redundant functions of the PI3K isoforms

Signal transduction and chemotaxis in mast cells

Mast cell plasticity and sphingosine-1-phosphate in immunity, inflammation and cancer

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