{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:41:41Z","timestamp":1791268901422,"version":"4.1.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2001,9,1]],"date-time":"2001-09-01T00:00:00Z","timestamp":999302400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>To prevent complement-mediated autologous tissue damage, host cells express a number of membrane-bound complement inhibitors. Decay-accelerating factor (DAF, CD55) is a GPI-linked membrane complement regulator that is widely expressed in mammalian tissues including the kidney. DAF inhibits the C3 convertase of both the classical and alternative pathways. Although DAF deficiency contributes to the human hematological syndrome paroxysmal nocturnal hemoglobinuria, the relevance of DAF in autoimmune tissue damage such as immune glomerulonephritis remains to be determined. In this study, we have investigated the susceptibility of knockout mice that are deficient in GPI-anchored DAF to nephrotoxic serum nephritis. Injection of a subnephritogenic dose of rabbit anti-mouse glomerular basement membrane serum induced glomerular disease in DAF knockout mice but not in wild-type controls. When examined at 8 days after anti-glomerular basement membrane treatment, DAF knockout mice had a much higher percentage of diseased glomeruli than wild-type mice (68.8 \u00b1 25.0 vs 10.0 \u00b1 3.5%; p &amp;lt; 0.01). Morphologically, DAF knockout mice displayed increased glomerular volume (516 \u00b1 68 vs 325 \u00b1 18 \u00d7 103 \u03bcm3 per glomerulus; p &amp;lt; 0.0001) and cellularity (47.1 \u00b1 8.9 vs 32.0 \u00b1 3.1 cells per glomerulus; p &amp;lt; 0.01). Although the blood urea nitrogen level showed no difference between the two groups, proteinuria was observed in the knockout mice but not in the wild-type mice (1.4 \u00b1 0.7 vs 0.02 \u00b1 0.01 mg\/24 h albumin excretion). The morphological and functional abnormalities in the knockout mouse kidney were associated with evidence of increased complement activation in the glomeruli. These results support the conclusion that membrane C3 convertase inhibitors like DAF play a protective role in complement-mediated immune glomerular damage in vivo.<\/jats:p>","DOI":"10.4049\/jimmunol.167.5.2791","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:43:49Z","timestamp":1398023029000},"page":"2791-2797","source":"Crossref","is-referenced-by-count":65,"title":["Increased Susceptibility of Decay-Accelerating Factor Deficient Mice to Anti-Glomerular Basement Membrane Glomerulonephritis"],"prefix":"10.1093","volume":"167","author":[{"given":"Hajime","family":"Sogabe","sequence":"first","affiliation":[{"name":"Division of Nephrology and Endocrinology, University of Tokyo School of Medicine , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaomi","family":"Nangaku","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology, University of Tokyo School of Medicine , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshitaka","family":"Ishibashi","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology, University of Tokyo School of Medicine , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takehiko","family":"Wada","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology, University of Tokyo School of Medicine , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiro","family":"Fujita","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology, University of Tokyo School of Medicine , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiujun","family":"Sun","sequence":"additional","affiliation":[{"name":"Center for Experimental Therapeutics and Departmentof Pharmacology, University of Pennsylvania School of Medicine , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takashi","family":"Miwa","sequence":"additional","affiliation":[{"name":"Center for Experimental Therapeutics and Departmentof Pharmacology, University of Pennsylvania School of Medicine , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael P","family":"Madaio","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, University of Pennsylvania School of Medicine , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-Chao","family":"Song","sequence":"additional","affiliation":[{"name":"Center for Experimental Therapeutics and Departmentof Pharmacology, University of Pennsylvania School of Medicine , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,9,1]]},"reference":[{"key":"2026020208131163600_R1","volume-title":"The Human Complement System in Health and Disease","year":"1998"},{"key":"2026020208131163600_R2","first-page":"265","volume-title":"Crit. 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