HLA Tissue Typing Laboratory

Berlin, Germany

HLA Tissue Typing Laboratory

Berlin, Germany
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Gunther J.,Innsbruck Medical University | Resch T.,Innsbruck Medical University | Hackl H.,Innsbruck Medical University | Sattler A.,Charité - Medical University of Berlin | And 12 more authors.
Kidney International | Year: 2017

The definition of biological donor organ age rather than chronological age seems obvious for the establishment of a valid pre-transplant risk assessment. Therefore, we studied gene expression for candidate markers in 60 zero-hour kidney biopsies. Compared with 29 younger donors under age 55, 31 elderly donors age 55 and older had significant mRNA expression for immunoproteasome subunits (PSMB8, PSMB9 and PSMB10), HLA-DRB, and transcripts of the activating cytotoxicity receptor NKG2D. Gene expression was validated in an independent donor cohort consisting of 37 kidneys from donors 30 years and under (Group I), 75 kidneys from donors age 31-54 years (Group II) and 75 kidneys from donors age 55 and older (Group III). Significant gene induction was confirmed in kidneys from Group III for PSMB9 and PSMB10. Strikingly, transcripts of NKG2D had the significantly highest gene induction in Group III versus Group II and Group I. Similar results were obtained for CDKN2A, but not for telomere length. Both NKG2D and CDKN2A mRNA expression were significantly correlated with creatinine levels at 24 months after transplantation. Univariate regression analysis showed significant predictive power regarding graft function at 6 and 12 months for NKG2D and CDKN2A. However, only NKG2D remained significantly predictive in the multivariate model at 12 months. Thus, our results reveal novel candidate markers in aged renal allografts, which could be helpful in the assessment of organ quality. © 2017 International Society of Nephrology.

Lachmann N.,Charité - Medical University of Berlin | Lachmann N.,HLA Tissue Typing Laboratory | Todorova K.,Charité - Medical University of Berlin | Todorova K.,HLA Tissue Typing Laboratory | And 4 more authors.
Transfusion Medicine and Hemotherapy | Year: 2013

The detection of antibodies against the human leukocyte antigen (HLA) complex has become indispensable in every clinical practice. The development of solid-phase assays like the Luminex allows the standardized measurement of anti-HLA antibodies (HLAab) with high sensitivity, albeit the relevance for some clinical settings remains a matter of debate. In this review we aim to describe the principle of Luminex-based antibody detection, including two modifications that allow identifying solely complement-activating antibodies. We then describe three applications for Luminex: i) detection of HLAab preceding solid-organ transplantation and monitoring of donor-specific antibodies posttransplant as a risk factor for antibody-mediated rejection; ii) presence of HLAab in recipients as a risk for graft failure in hematopoietic stem cell transplantation, especially in haploidentical or mismatched transplantations; iii) role of HLAab in blood transfusion including refractory thrombocytopenia and selection of suitable platelet donors, transfusion-related lung injury after plasma transfusion, and immunization against HLA after red blood cell transfusion despite leukodepletion. Although the Luminex platform constitutes a potent technology for HLA antibody detection, some drawbacks require the well-educated analysis and interpretation of data in critical cases. In addition, Luminex has become an important tool to identify clinically relevant antibodies. © 2013 S. Karger GmbH, Freiburg.

Todorova K.,HLA Tissue Typing Laboratory | Zuber K.,HLA Tissue Typing Laboratory | Neuwirt P.,HLA Tissue Typing Laboratory | Arnold R.,Oncology and Tumorimmunology | And 3 more authors.
Tissue Antigens | Year: 2014

We report the new HLA-A*11:192 allele differing from A*11:01 by one nucleotide in exon 2. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

PubMed | HLA Tissue Typing Laboratory
Type: Journal Article | Journal: Tissue antigens | Year: 2014

We report the new HLA-A*11:192 allele differing from A*11:01 by one nucleotide in exon 2.

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