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RoBE SIGNED

Study of the role of BANK1 in antibody production and antibody-independent functions of B cells in SLE

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 RoBE project word cloud

Explore the words cloud of the RoBE project. It provides you a very rough idea of what is the project "RoBE" about.

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Project "RoBE" data sheet

The following table provides information about the project.

Coordinator
FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD 

Organization address
address: AVENIDA AMERICO VESPUCIO 15 EDIF S2
city: SEVILLA
postcode: 41092
website: www.juntadeandalucia.es/fundacionprogresoysalud

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Total cost 259˙398 €
 EC max contribution 259˙398 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-CAR
 Starting year 2019
 Duration (year-month-day) from 2019-09-16   to  2022-10-21

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD ES (SEVILLA) coordinator 259˙398.00

Map

 Project objective

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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