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231225s2018 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2018.02.009
|2 doi
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|a pubmed24n0937.xml
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|a (DE-627)NLM281354316
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|a (NLM)29477343
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|a (PII)S1521-6616(17)30333-9
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Liu, Long
|e verfasserin
|4 aut
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| 245 |
1 |
2 |
|a T cell exhaustion characterized by compromised MHC class I and II restricted cytotoxic activity associates with acute B lymphoblastic leukemia relapse after allogeneic hematopoietic stem cell transplantation
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|c 2018
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 01.07.2019
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|a Date Revised 10.12.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2018 Elsevier Inc. All rights reserved.
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|a Acute B lymphoblastic leukemia (B-ALL) relapse contributes predominantly to the mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). However, the mechanism of B-ALL relapse after allo-HSCT remains unknown. The eradication of leukemia after allo-HSCT largely relies on graft-versus-leukemia (GVL) effects mediated by donor T cells. T cell exhaustion, characterized by the increased expression of inhibitory receptors and impaired function, may suppress GVL effects. In this study, we evaluated whether T cell exhaustion was involved in B-ALL relapse after allo-HSCT. The results showed that CD4+ and CD8+ T cells exhibited increased coexpression of PD-1 and Tim-3, and compromised proliferative capacity, cytokine production and cytotoxic potentials in relapsed patients. Additionally, T cells at the tumor site were more easily exhausted than T cells in the peripheral blood. Moreover, the reversal of T cell exhaustion might correlate with effective anti-leukemic responses after reinduction. These results suggested that T cell exhaustion was associated with B-ALL relapse after allo-HSCT as well as its treatment outcome
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a Acute B lymphoblastic leukemia
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| 650 |
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4 |
|a Allogeneic hematopoietic stem cell transplantation
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| 650 |
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4 |
|a Relapse
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| 650 |
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4 |
|a T cell exhaustion
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| 650 |
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7 |
|a HAVCR2 protein, human
|2 NLM
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| 650 |
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7 |
|a Hepatitis A Virus Cellular Receptor 2
|2 NLM
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| 650 |
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7 |
|a Histocompatibility Antigens Class I
|2 NLM
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| 650 |
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7 |
|a Histocompatibility Antigens Class II
|2 NLM
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| 650 |
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7 |
|a Programmed Cell Death 1 Receptor
|2 NLM
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| 700 |
1 |
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|a Chang, Ying-Jun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Xu, Lan-Ping
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Xiao-Hui
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Yu
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, Kai-Yan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Huang, Xiao-Jun
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 190(2018) vom: 15. Mai, Seite 32-40
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:190
|g year:2018
|g day:15
|g month:05
|g pages:32-40
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2018.02.009
|3 Volltext
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|a AR
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|d 190
|j 2018
|b 15
|c 05
|h 32-40
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