Properdin binds independent of complement activation in an in vivo model of anti-glomerular basement membrane disease

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dc.contributor.author O'Flynn, Joseph
dc.contributor.author Kotimaa, Juha
dc.contributor.author Faber-Krol, Ria
dc.contributor.author Koekkoek, Karin
dc.contributor.author Klar-Mohamad, Ngaisah
dc.contributor.author Koudijs, Angela
dc.contributor.author Schwaeble, Wilhelm J.
dc.contributor.author Stover, Cordula
dc.contributor.author Daha, Mohamed R.
dc.contributor.author van Kooten, Cees
dc.date.accessioned 2019-11-30T22:55:15Z
dc.date.available 2021-12-17T22:02:49Z
dc.date.issued 2018-12
dc.identifier.citation O'Flynn , J , Kotimaa , J , Faber-Krol , R , Koekkoek , K , Klar-Mohamad , N , Koudijs , A , Schwaeble , W J , Stover , C , Daha , M R & van Kooten , C 2018 , ' Properdin binds independent of complement activation in an in vivo model of anti-glomerular basement membrane disease ' , Kidney International , vol. 94 , no. 6 , pp. 1141-1150 . https://doi.org/10.1016/j.kint.2018.06.030
dc.identifier.other PURE: 120208558
dc.identifier.other PURE UUID: 0e6ac283-ba4c-46da-8adb-95c55f50db1f
dc.identifier.other WOS: 000450435000015
dc.identifier.other Scopus: 85057072027
dc.identifier.other ORCID: /0000-0003-2158-0721/work/51806853
dc.identifier.uri http://hdl.handle.net/10138/307703
dc.description.abstract Properdin is the only known positive regulator of complement activation by stabilizing the alternative pathway convertase through C3 binding, thus prolonging its half-life. Recent in vitro studies suggest that properdin may act as a specific pattern recognition molecule. To better understand the role of properdin in vivo, we used an experimental model of acute anti-glomerular basement membrane disease with wild-type, C3-and properdin knockout mice. The model exhibited severe proteinuria, acute neutrophil infiltration and activation, classical and alternative pathway activation, and progressive glomerular deposition of properdin, C3 and C9. Although the acute renal injury was likely due to acute neutrophil activation, we found properdin deposition in C3-knockout mice that was not associated with IgG. Thus, properdin may deposit in injured tissues in vivo independent of its main ligand C3. en
dc.format.extent 10
dc.language.iso eng
dc.relation.ispartof Kidney International
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject alternative pathway
dc.subject C1q
dc.subject C3
dc.subject C5b-9
dc.subject classical pathway
dc.subject complement
dc.subject glomerulonephritis
dc.subject inflammation glomerular basement membrane
dc.subject properdin
dc.subject ALTERNATIVE PATHWAY
dc.subject FACTOR-H
dc.subject INDUCED ARTHRITIS
dc.subject C3B DEPOSITION
dc.subject INJURY
dc.subject MICE
dc.subject ANTIBODY
dc.subject CELLS
dc.subject AMPLIFICATION
dc.subject PROTECTION
dc.subject 3111 Biomedicine
dc.title Properdin binds independent of complement activation in an in vivo model of anti-glomerular basement membrane disease en
dc.type Article
dc.contributor.organization University of Helsinki
dc.contributor.organization Department of Bacteriology and Immunology
dc.contributor.organization Medicum
dc.description.reviewstatus Peer reviewed
dc.relation.doi https://doi.org/10.1016/j.kint.2018.06.030
dc.relation.issn 0085-2538
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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