한빛사 논문
Seungwon Ryu,1 Jae Woo Shin,1 Soie Kwon,2 Jiwon Lee,3 Yong Chul Kim,2 Yoe-Sik Bae,4,5 Yong-Soo Bae,4,5 Dong Ki Kim,2,6,7 Yon Su Kim,2,6,7 Seung Hee Yang,3,6 and Hye Young Kim1,8
1Laboratory of Mucosal Immunology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea. 2Department of Internal Medicine and 3Biomedical Research Institute, Seoul National University Hospital, Seoul, South Korea. 4SRC Center for Immune Research on Non-lymphoid Organs and 5Department of Biological Sciences, Sungkyunkwan University, Suwon, South Korea. 6Kidney Research Institute, 7Department of Internal Medicine, and 8Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul National University College of Medicine, Seoul, South Korea.
SHY and HYK are co–senior authors and contributed equally to this work.
Abstract
The roles of neutrophils in renal inflammation are currently unclear. On examining these cells in the unilateral ureteral obstruction murine model of chronic kidney disease, we found that the injured kidney bore a large and rapidly expanding population of neutrophils that expressed the eosinophil marker Siglec-F. We first verified that these cells were neutrophils. Siglec-F+ neutrophils were recently detected in several studies in other disease contexts. We then showed that a) these cells were derived from conventional neutrophils in the renal vasculature by TGF-β1 and GM-CSF; b) they differed from their parent cells by more frequent hypersegmentation, higher expression of profibrotic inflammatory cytokines, and notably, expression of collagen 1; and c) their depletion reduced collagen deposition and disease progression, but adoptive transfer increased renal fibrosis. These findings have thus unveiled a subtype of neutrophils that participate in renal fibrosis and a potentially new therapeutic target in chronic kidney disease.
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