{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T19:22:00Z","timestamp":1767986520753,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,11,1]],"date-time":"2022-11-01T00:00:00Z","timestamp":1667260800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["HLA"],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:p>Antibodies against Rho GDP\u2010dissociation inhibitor 2 (RhoGDI2) are associated with inferior graft survival in transplant patients receiving a kidney from deceased donors. Although this suggests that these antibodies contribute to graft injury because of ischemia, it remains unknown whether they are also pathogenically involved in the process of graft loss. To study this, we firstly analyzed the IgG subclass profile of anti\u2010RhoGDI2 antibodies in kidney transplant recipients, and whether antibody titers change over time or because of acute rejection. Next, we investigated the expression of RhoGDI2 on primary kidney and lung endothelial cells (ECs) upon hypoxia reperfusion. In addition, the complement\u2010fixing properties of anti\u2010RhoGDI2 antibodies were studied using imaging flow cytometry. Anti\u2010RhoGDI2 antibodies in patients are mainly IgG1, and titers remained stable and seemed not be changed because of rejection. Antibodies against RhoGDI2, which surface expression seemed to increase upon hypoxia reperfusion, co\u2010localized with C3 on ECs. Binding of human IgG1 monoclonal anti\u2010RhoGDI2 antibodies as well as patient derived antibodies, resulted in complement activation, suggesting that these antibodies are complement fixing. This study suggested a potential pathogenic role of anti\u2010RhoGDI2 antibodies in kidney graft loss. During ischemia reperfusion, the ability of these antibodies to fix complement could be one of the mechanisms resulting in tissue injury.<\/jats:p>","DOI":"10.1111\/tan.14858","type":"journal-article","created":{"date-parts":[[2022,10,21]],"date-time":"2022-10-21T04:41:02Z","timestamp":1666327262000},"page":"103-114","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Complement component <scp>C3<\/scp> and C5b\u20109 deposition on hypoxia reperfused endothelial cells by <scp>non\u2010HLA<\/scp> antibodies against <scp>RhoGDI2<\/scp>: A player involved in graft failure?"],"prefix":"10.1111","volume":"101","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8736-4549","authenticated-orcid":false,"given":"Tineke","family":"Kardol\u2010Hoefnagel","sequence":"first","affiliation":[{"name":"Center for Translational Immunology University Medical Center Utrecht  Utrecht The 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