Pretransplant and posttransplant monitoring of anti-HLA class I IgG1 antibodies by ELISA identifies patients at high risk of graft loss

Monteiro, Francisco; Mineiro, Carlos; Rodrigues, H.; Paula, Flávio Jota de; Kalil, Jorge

doi:10.1016/s0041-1345(96)00541-6

Cited by 14 publications

(7 citation statements)

References 3 publications

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“…Griffiths et al [37] have suggested that skewing of IgG presensitization toward IgG1, as assessed by the binding to target T cells in a flow cytometric assay, may be associated with inferior kidney allograft performance. These results are in line with earlier analyses demonstrating correlations between the enzyme-linked immunosorbent assay (ELISA) based detection of alloreactive IgG1 and adverse renal allograft outcomes [38,39]. Discussing limited numbers of cases, some authors have also suggested a contribution of (complement-fixing) IgG3 [40] or even noncomplement-fixing IgG subclasses to rejection [41,42].…”

Section: Clinical Relevance Of Alloreactive Immunoglobulin Isotypes Asupporting

confidence: 86%

Antibodies, isotypes and complement in allograft rejection

Böhmig

Bartel²,

Wahrmann³

2008

Current Opinion in Organ Transplantation

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Section: Clinical Relevance Of Alloreactive Immunoglobulin Isotypes Asupporting

confidence: 86%

Antibodies, isotypes and complement in allograft rejection

Böhmig

Bartel²,

Wahrmann³

2008

Current Opinion in Organ Transplantation

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“…12,[22][23][24][25][26][27][28] The initial appearance of strong complementfixing IgG1 and IgG3 antibodies may expand to weak or noncomplement-binding IgG2 and IgG4 antibodies; therefore, various profiles of IgG subclasses are seen in transplant recipients. 29 Previous studies have failed to firmly identify a predictive subclass pattern due to the heterogeneous IgG subclass response and to several technical [30][31][32] and methodological limitations, mainly related to the small number of recipients included 26,33,34 or the lack of precise clinical and histologic phenotyping of the ABMR injury. 23,24 The integration of different properties of circulating anti-HLA DSA, including HLA class specificity, strength, complementbinding capacity and IgG subclasses, allowed us to identify three distinct clinical and histologic patterns of antibody-mediated injury, as recognized by the latest Banff classification: aABMR, sABMR, and ABMR-free.…”

Section: Discussionmentioning

confidence: 99%

IgG Donor-Specific Anti-Human HLA Antibody Subclasses and Kidney Allograft Antibody-Mediated Injury

Lefaucheur

Viglietti

Bentlejewski

et al. 2016

Journal of the American Society of Nephrology

246

234

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Antibodies may have different pathogenicities according to IgG subclass. We investigated the association between IgG subclasses of circulating anti-human HLA antibodies and antibody-mediated kidney allograft injury. Among 635 consecutive kidney transplantations performed between 2008 and 2010, we enrolled 125 patients with donorspecific anti-human HLA antibodies (DSA) detected in the first year post-transplant. We assessed DSA characteristics, including specificity, HLA class specificity, mean fluorescence intensity (MFI), C1q-binding, and IgG subclass, and graft injury phenotype at the time of sera evaluation. Overall, 51 (40.8%) patients had acute antibody-mediated rejection (aABMR), 36 (28.8%) patients had subclinical ABMR (sABMR), and 38 (30.4%) patients were ABMR-free. The MFI of the immunodominant DSA (iDSA, the DSA with the highest MFI level) was 67246464, and 41.6% of patients had iDSA showing C1q positivity. The distribution of iDSA IgG1-4 subclasses among the population was 75.2%, 44.0%, 28.0%, and 26.4%, respectively. An unsupervised principal component analysis integrating iDSA IgG subclasses revealed aABMR was mainly driven by IgG3 iDSA, whereas sABMR was driven by IgG4 iDSA. IgG3 iDSA was associated with a shorter time to rejection (P,0.001), increased microcirculation injury (P=0.002), and C4d capillary deposition (P,0.001). IgG4 iDSA was associated with later allograft injury with increased allograft glomerulopathy and interstitial fibrosis/tubular atrophy lesions (P,0.001 for all comparisons). Integrating iDSA HLA class specificity, MFI level, C1q-binding status, and IgG subclasses in a Cox survival model revealed IgG3 iDSA and C1q-binding iDSA were strongly and independently associated with allograft failure. These results suggest IgG iDSA subclasses identify distinct phenotypes of kidney allograft antibody-mediated injury.

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“…Patients who produce anti-HLA antibodies post kidney transplantation manifest more late graft dysfunction and graft loss (65,68,76,77). Graft survival in patients with anti-HLA antibodies detected by complement-dependent cytotoxicity, ELISA assay, and flow cytometry is reduced (65,68,70,72,74,75,(77)(78)(79)(80)(81).…”

Section: Anti-hla Antibodies Associated With Late Graft Deteriorationmentioning

confidence: 99%

The role of B cells and alloantibody in the host response to human organ allografts

Vongwiwatana

Tasanarong

Hidalgo

et al. 2003

Immunological Reviews

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Some human organ transplants deteriorate slowly over a period of years, often developing characteristic syndromes: transplant glomerulopathy (TG) in kidneys, bronchiolitis obliterans in lungs, and coronary artery disease in hearts. In the past, we attributed late graft deterioration to "chronic rejection", a distinct but mysterious immunologic process different from conventional rejection. However, it is likely that much of chronic rejection is explained by conventional T-cell-mediated rejection (TMR), antibody-mediated rejection (AMR), and other insults. Recently, criteria have emerged to now permit us to diagnose AMR in kidney transplants, particularly C4d deposition in peritubular capillaries and circulating antibody against donor human leukocyte antigens (HLA). Some cases with AMR develop TG, although the relationship of TG to AMR is complex. Thus, a specific diagnosis of AMR in kidney can now be made, based on graft damage, C4d deposition, and donor-specific alloantibodies. Criteria for AMR in other organs must be defined. Not all late rejections are AMR; some deteriorating organs probably have smoldering TMR. The diagnosis of late ongoing AMR raises the possibility of treatment to suppress the alloantibody, but efficacy of the available treatments requires further study.

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Pretransplant and posttransplant monitoring of anti-HLA class I IgG1 antibodies by ELISA identifies patients at high risk of graft loss

Cited by 14 publications

References 3 publications

Antibodies, isotypes and complement in allograft rejection

Antibodies, isotypes and complement in allograft rejection

IgG Donor-Specific Anti-Human HLA Antibody Subclasses and Kidney Allograft Antibody-Mediated Injury

The role of B cells and alloantibody in the host response to human organ allografts

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