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

Project description

Regulation of immune system hyperactivation in lupus

In autoimmune diseases the immune system mistakenly attacks its own healthy tissues and organs. Systemic lupus erythematosus (SLE) is associated with B cell dysfunction and production of autoantibodies, leading to heterogeneous clinical phenotypes. However, little is known about the regulatory mechanisms in place driving aberrant B cell function in SLE. To answer this question, researchers of the EU-funded RoBE project will focus on the B cell protein BANK1, which has a putative role in B cell hyperactivation. They will use a mouse model of SLE to study the implication of BANK1 in B cell activation and effector function. Apart from fundamental insight into the pathophysiology of autoimmunity, results will pave the way towards novel therapeutic interventions.

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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MSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)

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Call for proposal

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(opens in new window) H2020-MSCA-IF-2018

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Coordinator

FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD M.P.
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 259 398,72
Address
AVENIDA AMERICO VESPUCIO 15 EDIF S2
41092 Sevilla
Spain

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Region
Sur Andalucía Sevilla
Activity type
Research Organisations
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 259 398,72
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