Monthly Archives - June 2017

LABScan3D™ Multiplex Flow Analyze

LABScan3D™ & LABScan™ 100 SystemsThe new technology from One Lambda Inc. which Delta Laboratory Co. Ltd. is overwhelming to offer to lovely customers.

State of the art optics, electronics, and software make the LABScan systems capable of rapidly processing up to 96 samples. The LABScan3D and LABScan 100 systems are based on Luminex® xMAP® technology and use Luminex® xPONENT® software for data acquisition. Using the LABScan systems with our LABType™ and LABScreen™ family of products allows the user to make assignments of HLA antibodies as well as HLA typing with the analysis support of HLA Fusion.

 

LABScan3D™ Multiplex Flow Analyze

FEATURES & BENEFITS

  • Advanced multiplexing and expanded coverage
  • Multiplex up to 500 unique beads for broader analyte detection
  • Compatible with classic Luminex-based assays along with the new LABType XR and CWD assays
  • State-of-the-art acquisition software

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Common and well-documented HLA alleles: 2012 update to the CWD catalogue.

Abstract

We have updated the catalogue of common and well-documented (CWD) human leukocyte antigen (HLA) alleles to reflect current understanding of the prevalence of specific allele sequences. The original CWD catalogue designated 721 alleles at the HLA-A, -B, -C, -DRB1, -DRB3/4/5, -DQA1, -DQB1, and -DPB1 loci in IMGT (IMmunoGeneTics)/HLA Database release 2.15.0 as being CWD. The updated CWD catalogue designates 1122 alleles at the HLA-A, -B, -C, -DRB1, -DRB3/4/5, -DQA1, -DQB1, -DPA1 and -DPB1 loci as being CWD, and represents 14.3% of the HLA alleles in IMGT/HLA Database release 3.9.0. In particular, we identified 415 of these alleles as being ‘common’ (having known frequencies) and 707 as being ‘well-documented’ on the basis of ~140,000 sequence-based typing observations and available HLA haplotype data. Using these allele prevalence data, we have also assigned CWD status to specific G and P designations. We identified 147/151 G groups and 290/415 P groups as being CWD. The CWD catalogue will be updated on a regular basis moving forward, and will incorporate changes to the IMGT/HLA Database as well as empirical data from the histocompatibility and immunogenetics community. This version 2.0.0 of the CWD catalogue is available online at cwd.immunogenomics.org, and will be integrated into the Allele Frequencies Net Database, the IMGT/HLA Database and National Marrow Donor Program’s bioinformatics web pages.

PMID: 23510415
PMCID: PMC3634360
DOI: 10.1111/tan.12093
Reference : PubMed
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IgG Donor-Specific Anti-Human HLA Antibody Subclasses and Kidney Allograft Antibody-Mediated Injury

Abstract

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 donor-specific 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 6724±464, 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.

Author information

1. Department of Nephrology and Kidney Transplantation, Saint-Louis Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; Paris Translational Research Center for Organ Transplantation, National Institute of Health and Medical Research, Mixed Research Unit-S970, Paris, France; carmen.lefaucheur@wanadoo.fr.
2. Department of Nephrology and Kidney Transplantation, Saint-Louis Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; Paris Translational Research Center for Organ Transplantation, National Institute of Health and Medical Research, Mixed Research Unit-S970, Paris, France;
3. University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania;
4. Paris Translational Research Center for Organ Transplantation, National Institute of Health and Medical Research, Mixed Research Unit-S970, Paris, France; Department of Pathology, Necker Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France;
5. Methodology Unit (Research team 3181), University Hospital de Besançon, Besançon, France;
6. Paris Translational Research Center for Organ Transplantation, National Institute of Health and Medical Research, Mixed Research Unit-S970, Paris, France;
7. Department of Pathology, Saint-Louis Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; and.
8. Department of Kidney Transplantation, Necker Hospital, Assitance Publique-Hôpitaux de Paris, Paris, France.
9. Department of Nephrology and Kidney Transplantation, Saint-Louis Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France;
10. Paris Translational Research Center for Organ Transplantation, National Institute of Health and Medical Research, Mixed Research Unit-S970, Paris, France; Department of Kidney Transplantation, Necker Hospital, Assitance Publique-Hôpitaux de Paris, Paris, France.

KEYWORDS:

acute allograft; immunology and pathology; kidney transplantation; rejection

PMID: 26293822
PMCID: PMC4696574
DOI: 10.1681/ASN.2014111120

Reference : PubMed

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C1q-fixing human leukocyte antigen assay in immunized renal patients: correlation between Luminex SAB-C1q and SAB-IgG

Abstract

BACKGROUND:

There is no consensus about the impact of thresholds of complement-fixing antibody assays. Recently, a C1q-SAB assay has been developed to identify complement-fixing HLA antibodies with high sensitivity and specificity. Our aim was to determine the correlation between IgG single antigens beads (SAB) and C1q-SAB assay results among patients on the renal waiting list.

PATIENTS AND METHODS:

Serum samples from immunized renal waiting list patients as well as negative and positive controls were valided by Luminex (LMX). These sera, which were positive for 166 antibody specificities, were tested for HLA class I in parallel by LMX-IgG and LMX-C1q.

RESULTS:

Comparison of antibody detection revealed no correlation based on median fluorescent intensity (MFI), levels between the IgG SAB and the C1qSAB assay (P > .05). IgG-positive sera with MFIs as low as 700 were able to fix C1q, whereas other sera with MFIs as high 14,500 did not. Furthermore, there appeared to be disparities in the profiles of class I antigens able to fix C1q-SAB. In our series, only 34% class I IgG SAB antibodies were also C1qSAB+. In several patients, we detected C1qSAB+ against IgGSAB- that was surely due to IgM antibodies. So, the C1qSAB assay detected IgM antibodies that fix complement.

CONCLUSION:

These data suggested that the C1q-SAB assay could be an important method to evaluate pretransplant virtual crossmatch and to define nonpermitted specificities (C1q-fixing) in kidney transplantation.

Author information : Department of Nephrology, University Hospital Virgen Arrixaca, Murcia, Spain.

PMID: 23146446
DOI: 10.1016/j.transproceed.2012.09.084

Reference : PubMed

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