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PI3K-in-tolerance

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PI3K delta role in dendritic cell antigen processing and presentation to control...

PI3K delta role in dendritic cell antigen processing and presentation to control gut tolerance PI3Ks controls important biological processes immunity controlling vesicular trafficking and cell signaling events triggered by pathogen recognition receptors (PRRs). The engagement of PRRs leading to DC antigen processing and pre... ver más

14/11/2021

QMUL

213K€

Presupuesto del proyecto: 213K€

Líder del proyecto

QUEEN MARY UNIVERSITY OF LONDON No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-11-14

MSCA-IF-2018: Individual Fellowships

I+D

Cerrada hace 6 años

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No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

QMUL

212.93K€ | Lider

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Duración del proyecto: 31 meses Fecha Inicio: 2019-04-10
Fecha Fin: 2021-11-14

Líder del proyecto

QUEEN MARY UNIVERSITY OF LONDON No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 213K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto PI3Ks controls important biological processes immunity controlling vesicular trafficking and cell signaling events triggered by pathogen recognition receptors (PRRs). The engagement of PRRs leading to DC antigen processing and presentation (APP) is essential for the bridge between innate and adaptive immunity. Thus, DCs are crucial for resistance against pathogens, while concurrently maintaining tolerance to the commensal microbiota and environmental antigens. Crohn’s disease (CD)-like pathology has been documented in patients with chronic granulomatous disease (CGD), originating from mutations in genes encoding NADPH oxidase (NOX2) subunits or RAC2 GTPase. Both PRR-activated NOX2 and RAC2 are critical for inducing phagosomal reactive oxygen species (ROS) linked to APP processes in the DC. Thus, that dysregulated PRR signalling and NOX2 activity in the DC phagosome, may be key steps involved in some of the pathology observed in CD. The PRR family member NOD2 senses muramyl dipeptide in bacteria. NOD2 was the first susceptibility gene identified for CD and associated with tolerance mechanisms mediating intestinal homeostasis to gut microbiota. Recently, interactions between NOD2 and microbiome were shown to stimulate Treg activity at the mucosal sites. Bacteria-derived outer membrane vesicles (OMVs) from gut commensal Bacteriodes fragilis induce mucosal tolerance by DC-intrinsic activation of NOD2 and enabling DCs to induce IL10 production from Tregs. It is known that OMVs require NOX2-induced ROS to be released for APP and presented by MHCII to activate CD4 Tregs. Our preliminary data shows that mice inactivated in the kinase domain of PI3K delta spontaneously develop colitis in the presence of an intestinal opportunistic pathogens and show defects in antigen presentation in DCs in vitro. Based on these results, I propose to investigate the DC-intrinsic PI3K role in APP functions that control gut tolerance in this animal model of colitis.

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