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The possible critical role of T-cell help in DSA-mediated graft loss
C. Süsal, A. Slavcev, L. Pham, M. Zeier, C. Morath,
Language English Country England, Great Britain
Document type Journal Article, Review
Grant support
NV16-27477A
MZ0
CEP Register
Digital library NLK
Full text - Article
NLK
Medline Complete (EBSCOhost)
from 2004-05-01
Wiley Free Content
from 1997 to 2021
ROAD: Directory of Open Access Scholarly Resources
from 1988
PubMed
29405445
DOI
10.1111/tri.13126
Knihovny.cz E-resources
- MeSH
- Ki-1 Antigen immunology MeSH
- Tissue Donors MeSH
- HLA Antigens immunology MeSH
- Immunosuppressive Agents MeSH
- Isoantibodies blood MeSH
- Cohort Studies MeSH
- Complement System Proteins MeSH
- Humans MeSH
- Mice MeSH
- Graft Survival immunology MeSH
- Antibodies immunology MeSH
- Graft Rejection immunology MeSH
- Renal Insufficiency blood immunology MeSH
- T-Lymphocytes immunology MeSH
- Kidney Transplantation MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
In this review, we discuss a possible central role of T-cell help in severe forms of graft damage mediated by donor-specific HLA antibodies (DSA). Some kidney transplant recipients with pretransplant DSA show a high graft failure rate, whereas in other patients DSA do not harm the transplanted kidney and in most cases, disappear shortly after transplantation. Analyzing 80 desensitized highly immunized kidney transplant recipients and another multicenter cohort of 385 patients with pretransplant HLA antibodies, we reported recently that an ongoing T-cell help from an activated immune system, as measured by an increased level of soluble CD30 in serum, might be necessary for the DSA to exert a deleterious effect. Patients positive for both pretransplant DSA and sCD30 appear to require special measures, such as the elimination of DSA from the circulation, potent immunosuppression, good HLA-matching, and intense post-transplant monitoring, whereas exclusion of DSA-positive patients from transplantation in the absence of high sCD30 may not be justified in all cases, even if the pretransplant DSA are strong and complement-activating.
Department of Immunogenetics Institute for Clinical and Experimental Medicine Prague Czech Republic
Division of Nephrology University of Heidelberg Heidelberg Germany
Institute of Immunology University of Heidelberg Heidelberg Germany
References provided by Crossref.org
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