期刊
BLOOD
卷 121, 期 3, 页码 530-536出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2012-05-434209
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资金
- Swedish Research Council
- Swedish Cancer Foundation
- Ellen, Walter and Lennart Hesselman Foundation
- Ollie and Elof Ericsson Foundation
- King Gustaf V:s 80-years Foundation
- Ake Wiberg Foundation
- Karolinska Institutet
IL-33 is a recently discovered cytokine involved in induction of Th2 responses and functions as an alarmin. Despite numerous recent studies targeting IL-33, its role in vivo is incompletely understood. Here we investigated inflammatory responses to intraperitoneal IL-33 injections in wild-type and mast cell-deficient mice. We found that wild-type mice, but not mast cell-deficient W-sh/W-sh mice, respond to IL-33 treatment with neutrophil infiltration to the peritoneum, whereas other investigated cell types remained unchanged. In W-sh/W-sh mice, the IL-33-induced innate neutrophil response could be rescued by local reconstitution with wild-type but not with T1/ST2(-/-) mast cells, demonstrating a mast cell-dependent mechanism. Furthermore, we found this mechanism to be partially dependent on mast cell-derived TNF, as we observed reduced neutrophil infiltration in W-sh/W-sh mice reconstituted with TNF-/- bone marrow-derived mast cells compared with those reconstituted with wild-type bone marrow-derived mast cells. In agreement with our in vivo findings, we demonstrate that humanneutrophils migrate toward the supernatant of IL-33-treated human mast cells. Taken together, our findings reveal that IL-33 activates mast cells in vivo to recruit neutrophils, a mechanism dependent on IL-33R expression on peritoneal mast cells. Mast cells activated in vivo by IL-33 probably play an important role in inflammatory reactions. (Blood. 2013;121(3):530-536)
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