The inhibitory receptors on NK cells and CTLs are upregulated in adult and adolescent patients with secondary hemophagocytic lymphohistiocytosis

Copyright © 2019. Published by Elsevier Inc.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 202(2019) vom: 01. Mai, Seite 18-28
1. Verfasser: Gao, Zhuo (VerfasserIn)
Weitere Verfasser: Wang, Yini, Wang, Jingshi, Zhang, Jia, Wang, Zhao
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2019
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Cytotoxic T lymphocytes Hemophagocytic lymphohistiocytosis Natural killer cells Surface receptors Antigens, CD HAVCR2 protein, human Hepatitis A Virus Cellular Receptor 2 KLRC1 protein, human mehr... KLRK1 protein, human NK Cell Lectin-Like Receptor Subfamily C NK Cell Lectin-Like Receptor Subfamily K PDCD1 protein, human Programmed Cell Death 1 Receptor Lymphocyte Activation Gene 3 Protein Lag3 protein, human
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245 1 4 |a The inhibitory receptors on NK cells and CTLs are upregulated in adult and adolescent patients with secondary hemophagocytic lymphohistiocytosis 
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520 |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 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Cytotoxic T lymphocytes 
650 4 |a Hemophagocytic lymphohistiocytosis 
650 4 |a Natural killer cells 
650 4 |a Surface receptors 
650 7 |a Antigens, CD  |2 NLM 
650 7 |a HAVCR2 protein, human  |2 NLM 
650 7 |a Hepatitis A Virus Cellular Receptor 2  |2 NLM 
650 7 |a KLRC1 protein, human  |2 NLM 
650 7 |a KLRK1 protein, human  |2 NLM 
650 7 |a NK Cell Lectin-Like Receptor Subfamily C  |2 NLM 
650 7 |a NK Cell Lectin-Like Receptor Subfamily K  |2 NLM 
650 7 |a PDCD1 protein, human  |2 NLM 
650 7 |a Programmed Cell Death 1 Receptor  |2 NLM 
650 7 |a Lymphocyte Activation Gene 3 Protein  |2 NLM 
650 7 |a Lag3 protein, human  |2 NLM 
700 1 |a Wang, Yini  |e verfasserin  |4 aut 
700 1 |a Wang, Jingshi  |e verfasserin  |4 aut 
700 1 |a Zhang, Jia  |e verfasserin  |4 aut 
700 1 |a Wang, Zhao  |e verfasserin  |4 aut 
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