Non-HLA agonistic anti-angiotensin II type 1 receptor antibodies induce a distinctive phenotype of antibody-mediated rejection in kidney transplant recipients

Lefaucheur, Carmen; Viglietti, Denis; Bouatou, Yassine; Philippe, Aurélie; Pievani, Daniele; Aubert, Olivier; Huyen, Jean–Paul Duong Van; Taupin, Jean‐Luc; Glotz, Denis; Legendre, Christophe; Loupy, Alexandre; Halloran, Philip F.; Dragun, Duska

doi:10.1016/j.kint.2019.01.030

Cited by 125 publications

(143 citation statements)

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“…Diagnosis of mixed rejection and the often problematic coexistence of polyomavirus nephropathy and rejection or calcineurin inhibitor toxicity and rejection may benefit from this approach. Furthermore, clinical significance of antibody responses to non-HLA antigens, such as major histocompatibility complex class I chain-related proteins A and B and angiotensin II type 1 receptor, may be clarified [60,61].…”

Section: Future Perspectivesmentioning

confidence: 99%

Diagnosis of renal transplant rejection: Banff classification and beyond

Jeong

2020

Kidney Res Clin Pract

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Section: Future Perspectivesmentioning

confidence: 99%

Diagnosis of renal transplant rejection: Banff classification and beyond

Jeong

2020

Kidney Res Clin Pract

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“…Inflammatory cytokines IL‐8 and TNF‐α have been found increased in paediatric transplant patients with AT 1 R antibodies (Pearl et al., 2018). Patients with vascular rejection in the presence of AT 1 R antibodies have a higher occurrence of arterial inflammation (Lefaucheur et al., 2019).…”

Section: Mechanism Of Stimulation Of Non‐hla Antibodiesmentioning

confidence: 99%

Impact and production of Non‐HLA‐specific antibodies in solid organ transplantation

Zhang

Reinsmoen

2020

Int J Immunogenetics

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Abbreviations: AT 1 R, angiotensin II type 1 receptor; DSA, donor-specific antibody;ELISA, enzyme-linked immunosorbent assay; ET A R, endothelin type A receptor; FSGS, focal segmental glomerulosclerosis; GPCR, G protein-coupled receptor; HLA, human leucocyte antigen. AbstractOrgan transplantation is an effective way to treat end-stage organ disease. Extending the graft survival is one of the major goals in the modern era of organ transplantation. However, long-term graft survival has not significantly improved in recent years despite the improvement of patient management and advancement of immunosuppression regimen. Antibody-mediated rejection is a major obstacle for long-term graft survival. Donor human leucocyte antigen (HLA)-specific antibodies were initially identified as a major cause for antibody-mediated rejection. Recently, with the development of solid-phase-based assay reagents, the contribution of non-HLA antibodies in organ transplantation starts to be appreciated. Here, we review the role of most studied non-HLA antibodies, including angiotensin II type 1 receptor (AT 1 R), K-α-tubulin and vimentin antibodies, in the solid organ transplant, and discuss the possible mechanism by which these antibodies are stimulated. K E Y W O R D SAT 1 R, collagen V, HLA, K-α1-tubulin, non-HLA antibody, transplant, vimentin How to cite this article: Zhang X, Reinsmoen NL. Impact and production of Non-HLA-specific antibodies in solid organ transplantation. Int J Immunogenet. 2020;47:235-242.

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“…AT1R is expressed on the endothelium and represents a G‐protein‐coupled receptor such that antibodies interacting with the receptor activate signaling pathways . A recent study reported an HLA‐DSA‐independent effect on allograft rejection with a distinct histopathological (endothelial activation) and clinical phenotype (hypertension) . The endothelin receptor type A (ETAR) represents another G‐protein‐coupled receptor that has been identified as endothelial antigen.…”

Section: Non‐hla Antibody Responsementioning

confidence: 99%

Novel insights into non‐HLA alloimmunity in kidney transplantation

et al. 2019

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Recognition of non-self structures on donor cells represents the main immunological barrier in solid organ transplantation. The human leukocyte antigens (HLA) are considered the most important non-self (allo)antigens in transplantation. Long-term graft attrition is mainly caused by the formation of alloreactive antibodies that are directed against nonself structures (i.e., epitopes) on cell surface proteins. Recently published data provided evidence for a similar importance of non-HLA mismatches between donors and recipients in acute rejection as well as long-term kidney allograft survival. These data suggest a broader concept of immunological non-self that goes beyond HLA incompatibility and expands the current concept of polymorphic non-self epitopes on cell surface molecules from HLA to non-HLA targets. Amino acid substitutions caused by single nucleotide variants in protein-coding genes or complete loss of gene expression represent the basis for polymorphic residues in both HLA and non-HLA molecules. To better understand these novel insights in non-HLA alloimmunity, we will first review basic principles of the alloimmune response with a focus on the HLA epitope concept in donor-specific antibody formation before discussing key publications on non-HLA antibodies.

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Non-HLA agonistic anti-angiotensin II type 1 receptor antibodies induce a distinctive phenotype of antibody-mediated rejection in kidney transplant recipients

Cited by 125 publications

References 52 publications

Diagnosis of renal transplant rejection: Banff classification and beyond

Diagnosis of renal transplant rejection: Banff classification and beyond

Impact and production of Non‐HLA‐specific antibodies in solid organ transplantation

Novel insights into non‐HLA alloimmunity in kidney transplantation

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