TY - JOUR
T1 - Antibodies against Angiotensin II Type 1 and Endothelin A Receptors
T2 - Relevance and pathogenicity
AU - Philogene, Mary Carmelle
AU - Johnson, Tory
AU - Vaught, Arthur Jason
AU - Zakaria, Sammy
AU - Fedarko, Neal
N1 - Publisher Copyright:
© 2019 American Society for Histocompatibility and Immunogenetics
PY - 2019/8
Y1 - 2019/8
N2 - Antibodies against two G-protein coupled receptors (GPCRs), angiotensin II type 1 receptor (AT1R) and endothelin A receptor (ETAR) are among a growing number of autoantibodies that are found to be associated with allograft dysfunction. AT1R antibodies (AT1Rabs) and ETAR antibodies (ETARabs) have been shown to activate their target receptors and affect signaling pathways. Multiple single center reports have shown an association between presence of these antibodies and acute or chronic rejection and graft loss in kidney, heart, liver, lung and composite tissue transplantations. However, the characteristics of patients that are most likely to develop adverse outcomes, the phenotypes associated with graft damage solely due to these antibodies, and the antibody titer required to cause dysfunction are areas that remain controversial. This review compiles existing knowledge on the effect of antibodies against GPCRs in other diseases in order to bridge the gap in knowledge within transplantation biology. Future areas for research are highlighted and include the need for functional assays and treatment protocols for transplant patients who present with AT1Rabs and ETARabs. Understanding how antibodies that activate GPCRs influence transplantation outcome will have direct clinical implications for preemptive evaluation of transplant candidates as well as the post-transplant care of organ recipients.
AB - Antibodies against two G-protein coupled receptors (GPCRs), angiotensin II type 1 receptor (AT1R) and endothelin A receptor (ETAR) are among a growing number of autoantibodies that are found to be associated with allograft dysfunction. AT1R antibodies (AT1Rabs) and ETAR antibodies (ETARabs) have been shown to activate their target receptors and affect signaling pathways. Multiple single center reports have shown an association between presence of these antibodies and acute or chronic rejection and graft loss in kidney, heart, liver, lung and composite tissue transplantations. However, the characteristics of patients that are most likely to develop adverse outcomes, the phenotypes associated with graft damage solely due to these antibodies, and the antibody titer required to cause dysfunction are areas that remain controversial. This review compiles existing knowledge on the effect of antibodies against GPCRs in other diseases in order to bridge the gap in knowledge within transplantation biology. Future areas for research are highlighted and include the need for functional assays and treatment protocols for transplant patients who present with AT1Rabs and ETARabs. Understanding how antibodies that activate GPCRs influence transplantation outcome will have direct clinical implications for preemptive evaluation of transplant candidates as well as the post-transplant care of organ recipients.
KW - Allograft dysfunction
KW - Angiotensin II type 1 receptor antibody
KW - Endothelin A receptor antibody
KW - Non-HLA antibodies
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UR - http://www.scopus.com/inward/citedby.url?scp=85064407843&partnerID=8YFLogxK
U2 - 10.1016/j.humimm.2019.04.012
DO - 10.1016/j.humimm.2019.04.012
M3 - Review article
C2 - 31010696
AN - SCOPUS:85064407843
SN - 0198-8859
VL - 80
SP - 561
EP - 567
JO - Human Immunology
JF - Human Immunology
IS - 8
ER -