Inflammatory CD11c+ B Cells Induced by the TREM2 Signal Accelerate Sepsis Development.

Abstract

CD11c+ B cells are an age-associated subset emerging in infections and autoimmune diseases. However, their role in sepsis is poorly clarified. This study identified a class of CD11c+ B cells with a proinflammatory phenotype that is expended in septic patients and mice. Notably, the transfer of these cells accelerates sepsis-induced lung injury and death in mice. Furthermore, the CD11c+ B cells were induced by the triggering receptor expressed on myeloid cells 2 (TREM2) signal, which promotes their generation via the interferon regulatory factor 4 (IRF4) pathway. Moreover, TREM2 directly participates in sepsis regulation mediated by CD11c+ B cells. This study reveals the proinflammatory role of CD11c+ B cells in sepsis and identifies TREM2 as a contributing factor in CD11c+ B-cell-mediated inflammatory injury during sepsis.