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20240822232618.0 |
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240419s2024 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2024.110223
|2 doi
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|a pubmed24n1509.xml
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|a (DE-627)NLM371258707
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|a (NLM)38636890
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|a (PII)S1521-6616(24)00114-1
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Long, Jie
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Bone marrow CD8+ Trm cells induced by IL-15 and CD16+ monocytes contribute to HSPC destruction in human severe aplastic anemia
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 17.05.2024
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|a Date Revised 22.08.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2024 Elsevier Inc. All rights reserved.
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|a Idiopathic severe aplastic anemia (SAA) is a disease of bone marrow failure caused by T-cell-induced destruction of hematopoietic stem and progenitor cells (HSPCs), however the mechanism remains unclear. We performed single-cell RNA sequencing of PBMCs and BMMCs from SAA patients and healthy donors and identified a CD8+ T cell subset with a tissue residency phenotype (Trm) in bone marrow that exhibit high IFN-γ and FasL expression and have a higher ability to induce apoptosis in HSPCs in vitro through FasL expression. CD8+ Trm cells were induced by IL-15 presented by IL-15Rα on monocytes, especially CD16+ monocytes, which were increased in SAA patients. CD16+ monocytes contributed to IL-15-induced CD38+CXCR6+ pre-Trm differentiation into CD8+ Trm cells, which can be inhibited by the CD38 inhibitor 78c. Our results demonstrate that IL-15-induced CD8+ Trm cells are pathogenic cells that mediate HSPC destruction in SAA patients and are therapeutic targets for future treatments
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|a Journal Article
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|a Aplastic anemia
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| 650 |
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4 |
|a Bone marrow
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| 650 |
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4 |
|a Monocytes
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| 650 |
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|a Single cell RNA sequencing
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| 650 |
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4 |
|a Tissue resident memory CD8(+)T cell
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| 650 |
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|a IL15 protein, human
|2 NLM
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| 650 |
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|a FCGR3B protein, human
|2 NLM
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| 650 |
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|a FASLG protein, human
|2 NLM
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| 700 |
1 |
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|a You, Xing
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yang, Qiong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Song-Rong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhou, Ming
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhou, Wei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Caixia
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Xie, Huafeng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Yuping
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Shunqing
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lian, Zhe-Xiong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Liang
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 263(2024) vom: 21. Juni, Seite 110223
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:263
|g year:2024
|g day:21
|g month:06
|g pages:110223
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2024.110223
|3 Volltext
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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| 912 |
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|a GBV_ILN_24
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| 912 |
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|a GBV_ILN_350
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|a AR
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|d 263
|j 2024
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|h 110223
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