Non-HLA transplantation immunity revealed by lymphocytotoxic antibodies

Opelz, Gerhard

doi:10.1016/s0140-6736(05)66458-6

Cited by 298 publications

(190 citation statements)

References 17 publications

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“…On the other hand, accumulating evidence indicates that non-complement-fixing antibodies are also crucially involved in graft rejection via direct endothelial cell activation [31]. Independently, non-HLA antibodies have been demonstrated to play a major role in the pathogenesis of antibody-mediated rejection [32][33][34][35]. In particular, non-HLA antibodies against endothelial antigens such as the major histocompatibility complex class I-related chain A (MICA) cause antibody-mediated rejection in transplantation patients [36,37].…”

Section: Detection Of Hla Antibodiesmentioning

confidence: 99%

Acute and chronic antibody-mediated rejection in pediatric kidney transplantation

et al. 2014

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Acute antibody-mediated rejection is a diagnostic challenge in renal transplantation medicine. However, it is an important diagnosis to make, since chronic antibody-mediated rejection (CAMR) is the main cause of long-term graft loss. Antibody-mediated rejection is diagnosed by detecting donorspecific antibodies (DSAs) in the blood in combination with observing typical histomorphological signs in kidney biopsy, as described in the Banff classification. Therapy is based on the removal of DSAs by administering intravenous immunoglobulins (IVIGs), plasmapheresis, or immunoadsorption. Reoccurrence of antibodies is diminished by the use of rituximab, increased immunosuppression, and in some cases additional experimental substances. A combination of these techniques has been shown to be successful in the majority of cases of acute and chronic antibody-mediated rejection. Routine DSA monitoring is warranted for early detection of antibody-mediated rejection.

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Section: Detection Of Hla Antibodiesmentioning

confidence: 99%

Acute and chronic antibody-mediated rejection in pediatric kidney transplantation

et al. 2014

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“…8 Despite improved understanding of the assessment and monitoring for HLA mismatched epitopes, 8 the pathogenicity of donor-specific anti-HLA antibodies on CAI remains elusive. 9 This is shown with complete HLA matched transplants exhibiting finite survival due to progressive CAI, 10 and not infrequently, CAI observed in HLA mismatched grafts without demonstrable antibodies to donor-specific HLA antigens. 7 These findings strongly suggest that additional pathogenic antibodies drive the humoral axis of injury in CAI, 9,11 and may be the final common outcome.…”

mentioning

confidence: 99%

“…9 This is shown with complete HLA matched transplants exhibiting finite survival due to progressive CAI, 10 and not infrequently, CAI observed in HLA mismatched grafts without demonstrable antibodies to donor-specific HLA antigens. 7 These findings strongly suggest that additional pathogenic antibodies drive the humoral axis of injury in CAI, 9,11 and may be the final common outcome. The activation or transition of these non-HLA antibodies toward pathogenicity is likely through the underlying triggers of acute rejection, hypoperfusion, ischemia reperfusion, calcineurin toxicity, infection, and recurrent diseases.…”

mentioning

confidence: 99%

Non-HLA Antibodies to Immunogenic Epitopes Predict the Evolution of Chronic Renal Allograft Injury

Sigdel

Li²,

Tran³

et al. 2012

Journal of the American Society of Nephrology

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Chronic allograft injury (CAI) results from a humoral response to mismatches in immunogenic epitopes between the donor and recipient. Although alloantibodies against HLA antigens contribute to the pathogenesis of CAI, alloantibodies against non-HLA antigens likely contribute as well. Here, we used highdensity protein arrays to identify non-HLA antibodies in CAI and subsequently validated a subset in a cohort of 172 serum samples collected serially post-transplantation. There were 38 de novo non-HLA antibodies that significantly associated with the development of CAI (P,0.01) on protocol post-transplant biopsies, with enrichment of their corresponding antigens in the renal cortex. Baseline levels of preformed antibodies to MIG (also called CXCL9), ITAC (also called CXCL11), IFN-g, and glial-derived neurotrophic factor positively correlated with histologic injury at 24 months. Measuring levels of these four antibodies could help clinicians predict the development of CAI with .80% sensitivity and 100% specificity. In conclusion, pretransplant serum levels of a defined panel of alloantibodies targeting non-HLA immunogenic antigens associate with histologic CAI in the post-transplant period. Validation in a larger, prospective transplant cohort may lead to a noninvasive method to predict and monitor for CAI.

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“…This fact offers an explanation for the rejection of HLA-identical grafts. Indeed, transplant recipients from HLA-identical siblings with no PRA had considerably longer graft survival times in comparison to those who had anti-HLA antibodies (Opelz, 2005). The vascular endothelium of transplanted kidneys and other organs is the first line of defense between the allograft and the host immune system.…”

Section: Anti-endothelial Cells (Ec) Antibodiesmentioning

confidence: 99%

Characteristics, Detection, and Clinical Relevance of Alloantibodies in Kidney Transplantation

Lobashevsky¹

2011

Kidney Transplantation - New Perspectives

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Non-HLA transplantation immunity revealed by lymphocytotoxic antibodies

Cited by 298 publications

References 17 publications

Acute and chronic antibody-mediated rejection in pediatric kidney transplantation

Acute and chronic antibody-mediated rejection in pediatric kidney transplantation

Non-HLA Antibodies to Immunogenic Epitopes Predict the Evolution of Chronic Renal Allograft Injury

Characteristics, Detection, and Clinical Relevance of Alloantibodies in Kidney Transplantation

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