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20231225083514.0 |
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231225s2019 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2019.03.006
|2 doi
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|a pubmed24n0984.xml
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|a (DE-627)NLM29536601X
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|a (NLM)30914280
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|a (PII)S1521-6616(18)30532-1
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Gao, Zhuo
|e verfasserin
|4 aut
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|a The inhibitory receptors on NK cells and CTLs are upregulated in adult and adolescent patients with secondary hemophagocytic lymphohistiocytosis
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|c 2019
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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 13.02.2020
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|a Date Revised 07.12.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2019. Published by Elsevier Inc.
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|a Hemophagocytic lymphohistiocytosis (HLH) includes primary HLH (pHLH) and secondary HLH (sHLH). Mutations that cause abnormal functions in natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) are frequently identified in pHLH. However, why NK cells and CTLs exhibit abnormal functions in sHLH remains unclear. Here, we demonstrated that NK cells in sHLH exhibited a high expression of inhibitory receptor NKG2A and a low expression of activating receptor NKG2D. Besides, the expression of HLA-E on lymphocyte, the adaptor of NKG2A on NK cells, was elevated in sHLH. Moreover, CTLs in sHLH patients expressed a higher level of functional exhaustion markers PD-1, TIM-3 and LAG-3 as well as a lower secretion of IFN-γ and CD107a upon stimulation. In addition, the expression of MHC-I on lymphocytes was decreased. Taken together, our study indicates a potentially pathological mechanism of sHLH and may open up new avenues for the development of immunotherapies against sHLH
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Cytotoxic T lymphocytes
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|a Hemophagocytic lymphohistiocytosis
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|a Natural killer cells
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|a Surface receptors
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|a Antigens, CD
|2 NLM
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|a HAVCR2 protein, human
|2 NLM
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|a Hepatitis A Virus Cellular Receptor 2
|2 NLM
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650 |
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|a KLRC1 protein, human
|2 NLM
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7 |
|a KLRK1 protein, human
|2 NLM
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650 |
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7 |
|a NK Cell Lectin-Like Receptor Subfamily C
|2 NLM
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|a NK Cell Lectin-Like Receptor Subfamily K
|2 NLM
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|a PDCD1 protein, human
|2 NLM
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650 |
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|a Programmed Cell Death 1 Receptor
|2 NLM
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650 |
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|a Lymphocyte Activation Gene 3 Protein
|2 NLM
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|a Lag3 protein, human
|2 NLM
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700 |
1 |
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|a Wang, Yini
|e verfasserin
|4 aut
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700 |
1 |
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|a Wang, Jingshi
|e verfasserin
|4 aut
|
700 |
1 |
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|a Zhang, Jia
|e verfasserin
|4 aut
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700 |
1 |
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|a Wang, Zhao
|e verfasserin
|4 aut
|
773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 202(2019) vom: 01. Mai, Seite 18-28
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
8 |
|g volume:202
|g year:2019
|g day:01
|g month:05
|g pages:18-28
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856 |
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|u http://dx.doi.org/10.1016/j.clim.2019.03.006
|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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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 202
|j 2019
|b 01
|c 05
|h 18-28
|