The Potential Role of the Leucocyte Immunoglobulin-Like Receptors in Kidney Transplant Rejection: A Mini Review

Antibody-mediated rejection (ABMR) remains one of the main causes of long-term graft failure after kidney transplantation, despite the development of powerful immunosuppressive therapy. A detailed understanding of the complex interaction between recipient-derived immune cells and the allograft is th...

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Bibliographic Details
Published in:Transplant international 2024-07, Vol.37, p.12995
Main Authors: Palvair, Jovanne, Farhat, Imane, Chaintreuil, Mélanie, Dal Zuffo, Ludivine, Messager, Lennie, Tinel, Claire, Lamarthée, Baptiste
Format: Article
Language:English
Subjects:
allograft rejection
Animals
Antigens, CD - immunology
Graft Rejection - immunology
Health Archive
HLA Antigens - immunology
Humans
innate immunity
kidney transplant
Kidney Transplantation - adverse effects
LILRs
Macrophages - immunology
Mice
monocyte
Monocytes - immunology
Receptors, Immunologic - immunology
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Summary:Antibody-mediated rejection (ABMR) remains one of the main causes of long-term graft failure after kidney transplantation, despite the development of powerful immunosuppressive therapy. A detailed understanding of the complex interaction between recipient-derived immune cells and the allograft is therefore essential. Until recently, ABMR mechanisms were thought to be solely caused by adaptive immunity, namely, by anti-human leucocyte antigen (HLA) donor-specific antibody. However recent reports support other and/or additive mechanisms, designating monocytes/macrophages as innate immune contributors of ABMR histological lesions. In particular, in mouse models of experimental allograft rejection, monocytes/macrophages are readily able to discriminate non-self via paired immunoglobulin receptors (PIRs) and thus accelerate rejection. The human orthologs of PIRs are leukocyte immunoglobulin-like receptors (LILRs). Among those, LILRB3 has recently been reported as a potential binder of HLA class I molecules, shedding new light on LILRB3 potential as a myeloid mediator of allograft rejection. In this issue, we review the current data on the role of LILRB3 and discuss the potential mechanisms of its biological functions.
ISSN:1432-2277
0934-0874
1432-2277
DOI:10.3389/ti.2024.12995