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PO.1.2 Bank1 has a determinant role in the presence of age-associated b cells in autoimmunity
  1. G Gómez Hernández,
  2. M Morell Hita and
  3. M Alarcón Riquelme
  1. Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research (GENYO) ~ Granada ~ Spain


Systemic Lupus Erythematosus (SLE) is a multisystemic autoimmune disease characterized by the hyperactivity of B cells and the production of autoantibodies. Previous studies in our group described the genetic association between SLE and the B cell-specific gene BANK1. The role of BANK1 in disease progression remains unclear. Bank1 deficiency in mice ameliorates the lupus phenotype. It also reduces numbers of CXCR4hi T cells, known as extrafollicular T helper cells (Tefh), which are involved in autoantibody production. A B cell subpopulation rare in normal mice named known as Age-associated B cells (ABC) has been implicated in autoimmunity in both mice and humans (T-bet+ or DN2 cells). This population is thought to be driven by TLR7 signaling, secretes autoantibodies and increases with age. These ABC cells are expanded in lupus-prone mice while DN2 cells in lupus patients.

The main objective of this study was to determine the effect of Bank1 deficiency on the appearance of ABCs in an SLE model and the relationship of ABCs with Tefh. This project aims to define exactly which cells are producing the excess of proinflammatory cytokines and autoantibodies and what the role of BANK1 in this process is. In order to do that, we worked with two murine lupus models crossed with the knockout for Bank1, (Bank1-/-): a transgenic model of the TLR7 gene (, and a TLR7 pathway-induced disease model with Imiquimod (Imiquimod-induced model).

The results showed that Bank1 deficiency, in both models, decreased the total percentage of ABCs and Tefh. The lack of Bank1 also ameliorates signs of autoimmunity such as splenomegaly and the production of autoantibodies. Besides, it restores to normal the cellular phenotypes in the spleen modified by the autoimmune process.

Bank1 deficiency improves the development of the disease in both models and has an effect on the production of ABCs. In the absence of Bank1, the ABC number decreases and this reduction correlates positively with Tefh levels. Ongoing experiments are focused on understanding the role of Bank1 on the generation and differentiation of ABCs by in vitro and single-cell transcriptome assays.

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