Article | 27 August 2020

In the course of disease, TLR4 of the B lymphocyte membrane is stimulated by ligands to activate downstream NF-κB signaling, which eventually leads to the activation of B lymphocytes and their differentiation into plasma cells and then to the production of a large number of autoantibodies. The present work reveals that β-arr2 interacts with TLR4 and mediates its endocytosis, thus inhibiting downstream NF-κB signaling mediated by TLR4 and preventing B lymphocytes from overactivation and differentiation under stimulation with inflammatory mediators