Doke, TomohitoTomohitoDokeAbedini, AminAminAbediniAldridge, Daniel LDaniel LAldridgeYA-WEN YANGPark, JihwanJihwanParkHernandez, Christina MChristina MHernandezBalzer, Michael SMichael SBalzerShrestra, RojeshRojeshShrestraCoppock, GaiaGaiaCoppockRico, Juan M InclanJuan M InclanRicoHan, Seung YubSeung YubHanKim, JunhyongJunhyongKimXin, ShengShengXinPiliponsky, Adrian MAdrian MPiliponskyAngelozzi, MarcoMarcoAngelozziLefebvre, VeroniqueVeroniqueLefebvreSiracusa, Mark CMark CSiracusaHunter, Christopher AChristopher AHunterSusztak, KatalinKatalinSusztak2023-04-172023-04-172022-061529-2908https://scholars.lib.ntu.edu.tw/handle/123456789/630202Inflammation 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.enMAST-CELLS; EXPRESSION; INFLAMMATION; RECRUITMENT; ACTIVATION; BLEOMYCIN; INJURY; TISSUE; BETA; IL-6[SDGs]SDG3journal article10.1038/s41590-022-01200-7355525402-s2.0-85129882091WOS:000794083800001https://api.elsevier.com/content/abstract/scopus_id/85129882091