[HTML][HTML] IL-10–producing regulatory B10 cells inhibit intestinal injury in a mouse model

K Yanaba, A Yoshizaki, Y Asano, T Kadono… - The American journal of …, 2011 - Elsevier
K Yanaba, A Yoshizaki, Y Asano, T Kadono, TF Tedder, S Sato
The American journal of pathology, 2011Elsevier
B cells mediate multiple functions that influence immune and inflammatory responses. In
mice, the addition of dextran sulfate sodium (DSS) to drinking water leads to immediate
intestinal injury. Dextran sulfate sodium–induced intestinal injury serves as an experimental
animal model for human ulcerative colitis. The contribution of B cells to DSS-induced
intestinal injury is unclear. In this study, we show that DSS-induced intestinal injury was
more severe in CD19-deficient (CD19−/−) mice than in wild-type mice. These inflammatory …
B cells mediate multiple functions that influence immune and inflammatory responses. In mice, the addition of dextran sulfate sodium (DSS) to drinking water leads to immediate intestinal injury. Dextran sulfate sodium–induced intestinal injury serves as an experimental animal model for human ulcerative colitis. The contribution of B cells to DSS-induced intestinal injury is unclear. In this study, we show that DSS-induced intestinal injury was more severe in CD19-deficient (CD19−/−) mice than in wild-type mice. These inflammatory responses were negatively regulated by a unique IL-10–producing CD1dhiCD5+ regulatory B cell subset (B10 cells) that was absent in CD19−/− mice and represented only 1% to 2% of splenic B220+ cells in wild-type mice. Remarkably, adoptive transfer of these B10 cells from wild-type mice reduced inflammation in CD19−/− mice in an IL-10–dependent manner. These results demonstrate that IL-10 production from regulatory B10 cells regulates DSS-induced intestinal injury. These findings may provide new insights and therapeutic approaches for treating ulcerative colitis.
Elsevier