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Changes in the number and function of dendritic cells (DCs) have been reported to play an important role in endotoxin tolerance. It has been reported that expansion of splenic CD11c low CD45RB +  DCs occurs in mice injected with sublethal doses of lipopolysaccharide (LPS). However, the function of endotoxic shock-expanded CD11c low CD45RB +  DCs has not been examined. In this work, we show that endotoxic shock promotes the expansion of CD11c low CD45RB +  cells with dendritic morphology and the production of low levels of inflammatory cytokines and costimulatory molecules. The expanded cells induce the generation of regulatory T cells (Tregs), show incapability to stimulate T cells, and induce apoptosis of CD4 +  T cells  in vitro . As compared to CD11c hi CD45RB −  conventional DCs, the expanded cells exert better protection against colitis induction by CD4 +  CD25 −  T cells, even though both subpopulations show similar ability to induce Tregs  in vivo.  The better control of proinflammatory cytokine responses  in vivo  by the expanded cells is associated with more apoptosis in the Payer’s patches and in colonic tissue-infiltrating cells. Thus, the expanded cells can modulate inflammatory T cell responses through multiple mechanisms. Our study facilitates a better understanding how innate immune responses may shape adaptive immunity and immune suppression following LPS-induced acute inflammation.

Endotoxic shock-expanded murine CD11clowCD45RB+ regulatory dendritic cells modulate inflammatory T cell responses through multiple mechanisms