https://scholars.lib.ntu.edu.tw/handle/123456789/630202
標題: | Single-cell analysis identifies the interaction of altered renal tubules with basophils orchestrating kidney fibrosis | 作者: | Doke, Tomohito Abedini, Amin Aldridge, Daniel L YA-WEN YANG Park, Jihwan Hernandez, Christina M Balzer, Michael S Shrestra, Rojesh Coppock, Gaia Rico, Juan M Inclan Han, Seung Yub Kim, Junhyong Xin, Sheng Piliponsky, Adrian M Angelozzi, Marco Lefebvre, Veronique Siracusa, Mark C Hunter, Christopher A Susztak, Katalin |
關鍵字: | MAST-CELLS; EXPRESSION; INFLAMMATION; RECRUITMENT; ACTIVATION; BLEOMYCIN; INJURY; TISSUE; BETA; IL-6 | 公開日期: | 六月-2022 | 出版社: | NATURE PORTFOLIO | 卷: | 23 | 期: | 6 | 起(迄)頁: | 947 | 來源出版物: | Nature immunology | 摘要: | Inflammation is an important component of fibrosis but immune processes that orchestrate kidney fibrosis are not well understood. Here we apply single-cell sequencing to a mouse model of kidney fibrosis. We identify a subset of kidney tubule cells with a profibrotic-inflammatory phenotype characterized by the expression of cytokines and chemokines associated with immune cell recruitment. Receptor-ligand interaction analysis and experimental validation indicate that CXCL1 secreted by profibrotic tubules recruits CXCR2+ basophils. In mice, these basophils are an important source of interleukin-6 and recruitment of the TH17 subset of helper T cells. Genetic deletion or antibody-based depletion of basophils results in reduced renal fibrosis. Human kidney single-cell, bulk gene expression and immunostaining validate a function for basophils in patients with kidney fibrosis. Collectively, these studies identify basophils as contributors to the development of renal fibrosis and suggest that targeting these cells might be a useful clinical strategy to manage chronic kidney disease. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/630202 | ISSN: | 1529-2908 | DOI: | 10.1038/s41590-022-01200-7 |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。