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. 2024 Sep 3;3:1442006. doi: 10.3389/frtra.2024.1442006

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© 2024 Huelsboemer, Moscarelli, Dony, Boroumand, Kochen, Knoedler, Yu, Hauc, Stögner, Formica, Lian, Murphy, Pomahac and Kauke-Navarro.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) ABMR is thought to primarily involve the graft endothelium and to be mediated by endothelial binding of anti-HLA antibodies (donor specific antibodies) against HLA surface molecules expressed on endothelium that lines donor vasculature. This can lead to a chronic inflammatory process ultimately leading to allograft vasculopathy (43). (B) In VCA, DSA may lower the threshold for homing of alloreactive T-cells, thereby promoting acute cellular rejection. This may be mediated by increased expression of leukocyte-endothelial cell interactions via ICAM1, VCAM1, and Sele (increased expression seen in suspected ABMR of VCA) (39). (Created with Biorender.com).