Duffy and Kidd blood group antigens: minor histocompatibility antigens involved in renal allograft rejection?

Lerut, Evelyne; Damme, Boudewijn Van; Emonds, Marie‐Paule; Rouger, Philippe; Vanrenterghem, Yves; Pirenne, Jacques; Ansart‐Pirenne, Hélène

doi:10.1111/j.1537-2995.2007.01060.x

Cited by 58 publications

(42 citation statements)

References 50 publications

(48 reference statements)

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“…Moreover, to the extent that mHAs are shared on RBCs and solid organs, these data predict increased rejection of solid organs in multiply transfused patients, as it has been suggested in recent years. 36 Finally, as transfusion may induce memory cells specific for donor antigens, multiple transfusions may decrease efficacy of immunomodulatory approaches such as costimulatory blockade, which are less effective at inhibiting memory versus naive T cells. Extension of these studies into the human setting may consist of analyzing chronically transfused patients for T-cell immunity against known human mHAs through tetramer analysis of freshly isolated or restimulated peripheral T cells.…”

Section: Discussionmentioning

confidence: 99%

Minor histocompatibility antigens on transfused leukoreduced units of red blood cells induce bone marrow transplant rejection in a mouse model

Desmarets

Cadwell

Peterson

et al. 2009

Blood

111

173

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When successful, human leukocyte antigen (HLA)-matched bone marrow transplantation with reduced-intensity conditioning is a cure for several nonmalignant hematologic disorders that require chronic transfusion, such as sickle cell disease and aplastic anemia. However, there are unusually high bone marrow transplant (BMT) rejection rates in these patients. Rejection correlates with the number of transfusions before bone marrow transplantation, and it has been hypothesized that preimmunization to antigens on transfused blood may prime BMT rejection. Using a novel mouse model of red blood cell (RBC) transfusion and major histocompatibility complex-matched bone marrow transplantation, we report that transfusion of RBC products induced BMT rejection across minor histocompatibility antigen (mHA) barriers. It has been proposed that contaminating leukocytes are responsible for transfusion-induced BMT rejection; however, filter leukoreduction did not prevent rejection in the current studies. Moreover, we generated a novel transgenic mouse with RBC-specific expression of a model mHA and demonstrated that transfusion of RBCs induced a CD8 ؉ T-cell response. Together, these data suggest that mHAs on RBCs themselves are capable of inducing BMT rejection. Cellular immunization to mHAs is neither monitored nor managed by current transfusion medicine practice; however, the current data suggest that mHAs on RBCs may represent an unappreciated and significant consequence of RBC transfusion.

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Section: Discussionmentioning

confidence: 99%

Minor histocompatibility antigens on transfused leukoreduced units of red blood cells induce bone marrow transplant rejection in a mouse model

Desmarets

Cadwell

Peterson

et al. 2009

Blood

111

173

View full text Add to dashboard Cite

show abstract

“…Of note are the agonistic antibodies against the angiotensin II type 1 receptor (AT1R-AA) described in renal allograft recipients with severe vascular types of AR [72]. Antagonistic antibodies against MICA, the chemokine receptor Duffy, Kidd polymorphic blood group antigens and the most abundant heparin sulfate proteoglycan, Agrin, were associated with decreased allograft survival [50,73], chronic allograft damage [74] and the development of glomerulopathy [75]. …”

Section: Biomarkers Of Acute Allograft Rejectionmentioning

confidence: 99%

Biomarkers in solid organ transplantation: establishing personalized transplantation medicine

et al. 2011

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Technological advances in molecular and in silico research have enabled significant progress towards personalized transplantation medicine. It is now possible to conduct comprehensive biomarker development studies of transplant organ pathologies, correlating genomic, transcriptomic and proteomic information from donor and recipient with clinical and histological phenotypes. Translation of these advances to the clinical setting will allow assessment of an individual patient's risk of allograft damage or accommodation. Transplantation biomarkers are needed for active monitoring of immunosuppression, to reduce patient morbidity, and to improve long-term allograft function and life expectancy. Here, we highlight recent pre- and post-transplantation biomarkers of acute and chronic allograft damage or adaptation, focusing on peripheral blood-based methodologies for non-invasive application. We then critically discuss current findings with respect to their future application in routine clinical transplantation medicine. Complement-system-associated SNPs present potential biomarkers that may be used to indicate the baseline risk for allograft damage prior to transplantation. The detection of antibodies against novel, non-HLA, MICA antigens, and the expression of cytokine genes and proteins and cytotoxicity-related genes have been correlated with allograft damage and are potential post-transplantation biomarkers indicating allograft damage at the molecular level, although these do not have clinical relevance yet. Several multi-gene expression-based biomarker panels have been identified that accurately predicted graft accommodation in liver transplant recipients and may be developed into a predictive biomarker assay.

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“…Antibodies against MICA (MICA ϭ MHC class I polypeptide-related sequence A), a locus related to HLA determining a polymorphic series of antigens similar to HLA, have been associated with decreased graft survival (9,10). Duffy [a chemokine receptor, the Duffy antigen-receptor for chemokines (DARC)], and Kidd polymorphic blood group antigens, may be associated with chronic renal allograft histological injury (11). Antibodies against Agrin, the most abundant heparin sulfate proteoglycan present in the glomerular basal membrane, have been implicated in transplant glomerulopathy (12), and agonistic antibodies against the Angiotensin II type 1 receptor (AT 1 R-AA) were described in renal allograft recipients with severe vascular types of rejection and malignant hypertension (13).…”

mentioning

confidence: 99%

Identifying compartment-specific non-HLA targets after renal transplantation by integrating transcriptome and “antibodyome” measures

Li¹,

Wadia²,

Chen

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

141

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We have conducted an integrative genomics analysis of serological responses to non-HLA targets after renal transplantation, with the aim of identifying the tissue specificity and types of immunogenic non-HLA antigenic targets after transplantation. Posttransplant antibody responses were measured by paired comparative analysis of pretransplant and posttransplant serum samples from 18 pediatric renal transplant recipients, measured against 5,056 unique protein targets on the ProtoArray platform. The specificity of antibody responses were measured against gene expression levels specific to the kidney, and 2 other randomly selected organs (heart and pancreas), by integrated genomics, employing the mapping of transcription and ProtoArray platform measures, using AILUN. The likelihood of posttransplant non-HLA targets being recognized preferentially in any of 7 microdissected kidney compartments was also examined. In addition to HLA targets, non-HLA immune responses, including anti-MICA antibodies, were detected against kidney compartment-specific antigens, with highest posttransplant recognition for renal pelvis and cortex specific antigens. The compartment specificity of selected antibodies was confirmed by IHC. In conclusion, this study provides an immunogenic and anatomic roadmap of the most likely non-HLA antigens that can generate serological responses after renal transplantation. Correlation of the most significant non-HLA antibody responses with transplant health and dysfunction are currently underway.integrative genomics ͉ kidney compartment ͉ kidney transplantation ͉ non-HLA antigen

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Duffy and Kidd blood group antigens: minor histocompatibility antigens involved in renal allograft rejection?

Abstract: This renal model unmasks for the first time the role of FY and-to a lesser extent-JK antigens as minor histocompatibility antigens and suggests their potential role for other clinical transplant settings.

Cited by 58 publications

References 50 publications

Minor histocompatibility antigens on transfused leukoreduced units of red blood cells induce bone marrow transplant rejection in a mouse model

Minor histocompatibility antigens on transfused leukoreduced units of red blood cells induce bone marrow transplant rejection in a mouse model

Biomarkers in solid organ transplantation: establishing personalized transplantation medicine

Identifying compartment-specific non-HLA targets after renal transplantation by integrating transcriptome and “antibodyome” measures

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