scholarly journals IL-1β regulates a novel myeloid-derived suppressor cell subset that impairs NK cell development and function

2010 ◽  
Vol 40 (12) ◽  
pp. 3347-3357 ◽  
Author(s):  
Moshe Elkabets ◽  
Vera S. G. Ribeiro ◽  
Charles A. Dinarello ◽  
Suzanne Ostrand-Rosenberg ◽  
James P. Di Santo ◽  
...  
2019 ◽  
Vol 79 (15) ◽  
pp. 3891-3902
Author(s):  
Xian Huang ◽  
Yong Zuo ◽  
Xiuzhi Wang ◽  
Xuefeng Wu ◽  
Hongsheng Tan ◽  
...  

Blood ◽  
2018 ◽  
Vol 132 (17) ◽  
pp. 1792-1804 ◽  
Author(s):  
Steven D. Scoville ◽  
Ansel P. Nalin ◽  
Luxi Chen ◽  
Li Chen ◽  
Michael H. Zhang ◽  
...  

Key Points Human and murine AML activate the AHR pathway, which can regulate miR-29b expression and impair NK cell development and function. AML-induced impairment of NK cell development and function can be reversed with AHR antagonist.


2019 ◽  
Vol 115 ◽  
pp. 21-30 ◽  
Author(s):  
Alexander Vargas-Hernández ◽  
Lisa R. Forbes

2017 ◽  
Vol 177 ◽  
pp. 60-69 ◽  
Author(s):  
Jeffrey W. Leong ◽  
Julia A. Wagner ◽  
Aaron R. Ireland ◽  
Todd A. Fehniger

2006 ◽  
Vol 18 (8) ◽  
pp. 1305-1314 ◽  
Author(s):  
L. V. Fostel

2006 ◽  
Vol 203 (10) ◽  
pp. 2339-2350 ◽  
Author(s):  
Domenico Mavilio ◽  
Gabriella Lombardo ◽  
Audrey Kinter ◽  
Manuela Fogli ◽  
Andrea La Sala ◽  
...  

In this study, we demonstrate that the in vitro interactions between a CD56neg/CD16pos (CD56neg) subset of natural killer (NK) cells and autologous dendritic cells (DCs) from HIV-1–infected viremic but not aviremic individuals are markedly impaired and likely interfere with the development of an effective immune response. Among the defective interactions are abnormalities in the process of reciprocal NK–DC activation and maturation as well as a defect in the NK cell–mediated editing or elimination of immature DCs (iDCs). Notably, the lysis of mature DCs (mDCs) by autologous NK cells was highly impaired even after the complete masking of major histocompatibility complex I molecules, suggesting that the defective elimination of autologous iDCs is at the level of activating NK cell receptors. In this regard, the markedly impaired expression/secretion and function of NKp30 and TNF-related apoptosis-inducing ligand, particularly among the CD56neg NK cell subset, largely accounts for the highly defective NK cell–mediated lysis of autologous iDCs. Moreover, mDCs generated from HIV-1 viremic but not aviremic patients are substantially impaired in their ability to secrete interleukin (IL)-10 and -12 and to prime the proliferation of neighboring autologous NK cells, which, in turn, fail to secrete adequate amounts of interferon-γ.


2021 ◽  
Vol 12 ◽  
Author(s):  
Jingli Lu ◽  
Yan Liang ◽  
Haiyang Meng ◽  
Ailing Zhang ◽  
Junjie Zhao ◽  
...  

Forkhead box protein 3 (Foxp3+)-expressing regulatory T (Treg) cells are a unique CD4+T cell subset that suppresses excessive immune responses. The epigenetic plasticity and metabolic traits of Treg cells are crucial for the acquisition of their phenotypic and functional characteristics. Therefore, alterations to the epigenetics and metabolism affect Treg cell development and function. Recent evidence reveals that altering the metabolic pathways and generation of metabolites can regulate the epigenetics of Treg cells. Specifically, some intermediates of cell metabolism can directly act as substrates or cofactors of epigenetic-modifying enzymes. Here, we describe the metabolic and epigenetic features during Treg cell development, and discuss how metabolites can contribute to epigenetic alterations of Treg cells, which affects Treg cell activation, differentiation, and function.


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