Joel Wilmore

T-bet+ B cells have emerged as a major B cell subset associated with both protective immunity and immunopathogenesis. T-bet is a transcription factor associated with the type I adaptive immune response to intracellular pathogens, driving an effector program characterized by the production of IFN-γ. Murine infection with the intracellular bacterium, Ehrlichia muris, generates protective extrafollicular T cell–independent T-bet+ IgM-secreting plasmablasts, as well as T-bet+ IgM memory cells. Although T-bet is a signature transcription factor for this subset, it is dispensable for splenic CD11c+ memory B cell development, but not for class switching to IgG2c. In addition to the T-bet+ plasmablasts found in the spleen, we show that Ab-secreting cells can also be found within the mouse peritoneal cavity; these cells, as well as their CD138− counterparts, also expressed T-bet. A large fraction of the T-bet+ peritoneal B cells detected during early infection were highly proliferative and expressed CXCR3 and CD11b, but, unlike in the spleen, they did not express CD11c. T-bet+ CD11b+ memory B cells were the dominant B cell population in the peritoneal cavity at 30 d postinfection, and although they expressed high levels of T-bet, they did not require B cell–intrinsic T-bet expression for their generation. Our data uncover a niche for T-bet+ B cells within the peritoneal cavity during intracellular bacterial infection, and they identify this site as a reservoir for T-bet+ B cell memory.