-
Je něco špatně v tomto záznamu ?
The possible critical role of T-cell help in DSA-mediated graft loss
C. Süsal, A. Slavcev, L. Pham, M. Zeier, C. Morath,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, přehledy
Grantová podpora
NV16-27477A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
NLK
Medline Complete (EBSCOhost)
od 2004-05-01
Wiley Free Content
od 1997 do 2021
ROAD: Directory of Open Access Scholarly Resources
od 1988
PubMed
29405445
DOI
10.1111/tri.13126
Knihovny.cz E-zdroje
- MeSH
- antigen Ki-1 imunologie MeSH
- dárci tkání MeSH
- HLA antigeny imunologie MeSH
- imunosupresiva MeSH
- isoprotilátky krev MeSH
- kohortové studie MeSH
- komplement MeSH
- lidé MeSH
- myši MeSH
- přežívání štěpu imunologie MeSH
- protilátky imunologie MeSH
- rejekce štěpu imunologie MeSH
- renální insuficience krev imunologie MeSH
- T-lymfocyty imunologie MeSH
- transplantace ledvin MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy 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
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc19000936
- 003
- CZ-PrNML
- 005
- 20230207113011.0
- 007
- ta
- 008
- 190107s2018 enk f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1111/tri.13126 $2 doi
- 035 __
- $a (PubMed)29405445
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a enk
- 100 1_
- $a Süsal, Caner $u Institute of Immunology, University of Heidelberg, Heidelberg, Germany.
- 245 14
- $a The possible critical role of T-cell help in DSA-mediated graft loss / $c C. Süsal, A. Slavcev, L. Pham, M. Zeier, C. Morath,
- 520 9_
- $a 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.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a protilátky $x imunologie $7 D000906
- 650 _2
- $a kohortové studie $7 D015331
- 650 _2
- $a komplement $7 D003165
- 650 _2
- $a rejekce štěpu $x imunologie $7 D006084
- 650 _2
- $a přežívání štěpu $x imunologie $7 D006085
- 650 _2
- $a HLA antigeny $x imunologie $7 D006680
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a imunosupresiva $7 D007166
- 650 _2
- $a isoprotilátky $x krev $7 D007518
- 650 _2
- $a antigen Ki-1 $x imunologie $7 D017730
- 650 _2
- $a transplantace ledvin $7 D016030
- 650 _2
- $a myši $7 D051379
- 650 _2
- $a renální insuficience $x krev $x imunologie $7 D051437
- 650 _2
- $a T-lymfocyty $x imunologie $7 D013601
- 650 _2
- $a dárci tkání $7 D014019
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a přehledy $7 D016454
- 700 1_
- $a Slavcev, Antonij $u Department of Immunogenetics, Institute for Clinical and Experimental Medicine (IKEM), Prague, Czech Republic.
- 700 1_
- $a Pham, Lien $u Institute of Immunology, University of Heidelberg, Heidelberg, Germany.
- 700 1_
- $a Zeier, Martin $u Division of Nephrology, University of Heidelberg, Heidelberg, Germany. $7 xx0281649
- 700 1_
- $a Morath, Christian $u Division of Nephrology, University of Heidelberg, Heidelberg, Germany.
- 773 0_
- $w MED00004553 $t Transplant international $x 1432-2277 $g Roč. 31, č. 6 (2018), s. 577-584
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/29405445 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20190107 $b ABA008
- 991 __
- $a 20230207113007 $b ABA008
- 999 __
- $a ok $b bmc $g 1364905 $s 1039059
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2018 $b 31 $c 6 $d 577-584 $e 20180308 $i 1432-2277 $m Transplant international $n Transpl Int $x MED00004553
- GRA __
- $a NV16-27477A $p MZ0
- LZP __
- $a Pubmed-20190107