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Although neutrophils are known to play an important role in the progression of crescentic glomerulonephritis, such as anti\u2010neutrophil cytoplasmic antibody (ANCA)\u2010associated glomerulonephritis, the key chemoattractant for neutrophils in ANCA\u2010associated glomerulonephritis has not been identified. Here, we demonstrate that a lipid chemoattractant, leukotriene B\n                    <jats:sub>4<\/jats:sub>\n                    (LTB\n                    <jats:sub>4<\/jats:sub>\n                    ), and its receptor BLT1 are primarily involved in disease pathogenesis in a mouse model of immune complex\u2010mediated crescentic glomerulonephritis. Circulating neutrophils accumulated into glomeruli within 1\u2009h after disease onset, which was accompanied by LTB\n                    <jats:sub>4<\/jats:sub>\n                    accumulation in the kidney cortex, leading to kidney injury. LTB\n                    <jats:sub>4<\/jats:sub>\n                    was produced by cross\u2010linking of Fc gamma receptors on neutrophils. Mice deficient in BLT1 or LTB\n                    <jats:sub>4<\/jats:sub>\n                    biosynthesis exhibited suppressed initial neutrophil infiltration and subsequent thrombotic glomerulonephritis and renal fibrosis. Depletion of neutrophils before, but not after, disease onset prevented proteinuria and kidney injury, indicating the essential role of neutrophils in the early phase of glomerulonephritis. Administration of a BLT1 antagonist before and after disease onset almost completely suppressed induction of glomerulonephritis. Finally, we found that the glomeruli from patients with ANCA\u2010associated glomerulonephritis contained more BLT1\u2010positive cells than glomeruli from patients with other etiologies. Taken together, the LTB\n                    <jats:sub>4<\/jats:sub>\n                    \u2010BLT1 axis is the key driver of neutrophilic glomerular inflammation, and will be a novel therapeutic target for the crescentic glomerulonephritis.\n                  <\/jats:p>","DOI":"10.1096\/fj.202201936r","type":"journal-article","created":{"date-parts":[[2023,1,24]],"date-time":"2023-01-24T10:13:08Z","timestamp":1674555188000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["The leukotriene\n                    <scp>\n                      B\n                      <sub>4<\/sub>\n                    <\/scp>\n                    \/\n                    <scp>BLT1<\/scp>\n                    \u2010dependent neutrophil accumulation exacerbates immune complex\u2010mediated glomerulonephritis"],"prefix":"10.1096","volume":"37","author":[{"given":"Ryotaro","family":"Shioda","sequence":"first","affiliation":[{"name":"Department of Biochemistry Juntendo University Graduate School of Medicine  Tokyo Japan"},{"name":"Department of Nephrology Juntendo University Faculty of Medicine  Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Airi","family":"Jo\u2010Watanabe","sequence":"additional","affiliation":[{"name":"Department of Biochemistry Juntendo University Graduate School of Medicine  Tokyo Japan"},{"name":"AMED\u2010PRIME, Japan Agency for Medical Research and Development  Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0270-5744","authenticated-orcid":false,"given":"Toshiaki","family":"Okuno","sequence":"additional","affiliation":[{"name":"Department of Biochemistry Juntendo University Graduate School of Medicine  Tokyo 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