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Study of the role of BANK1 in antibody production and antibody independent funct...

Study of the role of BANK1 in antibody production and antibody independent functions of B cells in SLE Systemic Lupus Erythematosus (SLE, Lupus) is a life-threatening and incurable autoimmune disease that affects primarily women, its pathogenesis is related with an exaggerated B cells activation that results both in the generation... ver más

21/10/2022

FUNDACION PUBLICA...

259K€

Presupuesto del proyecto: 259K€

Líder del proyecto

FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 14M€

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2022-10-21

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

FUNDACION PUBLICA ANDALUZA P...

259.40K€ | Lider

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Duración del proyecto: 42 meses Fecha Inicio: 2019-03-22
Fecha Fin: 2022-10-21

Líder del proyecto

FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 14M€

Presupuesto del proyecto 259K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Systemic Lupus Erythematosus (SLE, Lupus) is a life-threatening and incurable autoimmune disease that affects primarily women, its pathogenesis is related with an exaggerated B cells activation that results both in the generation of antibodies against self-nuclear acid antigens and in the generation of subsets of B cells that can exert antibody-independent roles in Lupus. However, the mechanisms that regulate aberrant B cell functions are poorly understood. In this project, we propose to investigate the role of the B cell scaffold protein with ankyrin repeats 1 (BANK1) in the B cell activation signaling pathways in a mouse model of Lupus. We have previously reported that the absence of BANK1 signaling in mice susceptible to Lupus resulted in the reduction of the activation of B cells, circulating total IgG2c and IgG autoantibodies, pro-inflammatory cytokines, and transcription factors related with TLR7 activation. Our data suggest that BANK1 is an important mediator of B cell hyperactivation. We hypothesize that BANK1 plays an important role in B cell signaling affecting their activation and effector functions in Lupus, however we do not fully understand yet the mechanism behind the function of BANK1. Our specific aims are: 1) to define how BANK1 signaling drives class switch recombination, 2) to determine the mechanism by which BANK1 regulates the cytokine production in B cells, and 3) to examine the participation of BANK1 signaling in the differentiation of pathogenic B cell subsets. To accomplish our objectives, we will use flow and mass cytometry, RNA-based next-generation sequencing (RNA-seq) analysis, the assay for transposase-accessible chromatin followed by deep sequencing (ATAC-seq), and a chromatin immunoprecipitation (ChIP) assay. We expect that the results of these studies will help to understand the molecular mechanism underlying the pathogenic B cell response in Lupus and will lead to identification of new avenues for therapeutic development.

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