scholarly journals A critical role of toll-like receptor 4 (TLR4) and its’ in vivo ligands in basal radio-resistance

2013 ◽  
Vol 4 (5) ◽  
pp. e649-e649 ◽  
Author(s):  
C Liu ◽  
C Zhang ◽  
R EJ Mitchel ◽  
J Cui ◽  
J Lin ◽  
...  
2019 ◽  
Vol 315 ◽  
pp. 23-30 ◽  
Author(s):  
Yun-Jie Shi ◽  
Hai-Feng Gong ◽  
Quan-Quan Zhao ◽  
Xiao-Shuang Liu ◽  
Cong Liu ◽  
...  

Circulation ◽  
2002 ◽  
Vol 106 (15) ◽  
pp. 1985-1990 ◽  
Author(s):  
Aryan Vink ◽  
Arjan H. Schoneveld ◽  
Jelger J. van der Meer ◽  
Ben J. van Middelaar ◽  
Joost P.G. Sluijter ◽  
...  

2004 ◽  
Vol 78 (2) ◽  
pp. 576-584 ◽  
Author(s):  
Dalia Burzyn ◽  
John C. Rassa ◽  
David Kim ◽  
Irene Nepomnaschy ◽  
Susan R. Ross ◽  
...  

ABSTRACT Mouse mammary tumor virus (MMTV) is a milk-borne retrovirus that exploits the adaptive immune system. It has recently been shown that MMTV activates B cells via Toll-like receptor 4 (TLR4), a molecule involved in innate immune responses. Here, we show that direct virus binding to TLR4 induced maturation of bone marrow-derived dendritic cells and up-regulated expression of the MMTV entry receptor (CD71) on these cells. In vivo, MMTV increased the number of dendritic cells in neonatal Peyer's patches and their expression of CD71; both these effects were dependent on TLR4. Thus, retroviral signaling through TLRs plays a critical role in dendritic-cell participation during infection.


Author(s):  
Yangchun Hu ◽  
Chao Li ◽  
Xiaojian Wang ◽  
Weiwei Chen ◽  
Yu Qian ◽  
...  

Increasing evidence suggests that triggering receptor expressed on myeloid cells 2 (TREM2) is implicated in the pathophysiology of neuroinflammation. The aim here was to investigate the neuroprotective role of TREM2 and its regulatory mechanism after subarachnoid hemorrhage (SAH). TREM2 siRNA was administered to measure the detrimental role of TREM2 in mediating microglial polarization in vivo and in vitro after experimental SAH. The relationship between Toll-like receptor 4 (TLR4) signaling and TREM2 was further explored. The soluble TREM2 from the cerebrospinal fluid (CSF) of patients with SAH was detected. The results showed that TREM2 mainly located in the microglia and presented a markedly delayed elevation after SAH. TREM2 knockdown triggered increased pro-inflammatory productions, aggravated microglial activities, and further exacerbated neurological dysfunction after SAH. Significantly, TLR4 knockout increased the expression of TREM2, accompanied by ameliorated neuroinflammation and improved neurological function. Corresponding to different clinical Hunt–Hess grades, obviously enhanced accumulation of soluble TREM2 was detected in the CSF of patients with SAH. TREM2 played a pivotal role in mediating microglial polarization after SAH, and the neuroprotective effect of TREM2 might be potentially suppressed by the hyperactive TLR4 in the early phase of SAH. Pharmacological targeting of TREM2 may be a promising strategy for SAH therapy.


2019 ◽  
Vol 64 (3) ◽  
pp. 194-200
Author(s):  
Xiandong Zhan ◽  
Lijuan Wang ◽  
Zhenhui Wang ◽  
Shiping Chai ◽  
Xiaobo Zhu ◽  
...  

2020 ◽  
Vol 321 ◽  
pp. 54-60 ◽  
Author(s):  
Mingxin Dong ◽  
Haotian Yu ◽  
Yan Wang ◽  
Chengbiao Sun ◽  
Ying Chang ◽  
...  

2001 ◽  
Vol 183 (11) ◽  
pp. 1617-1624 ◽  
Author(s):  
Georg Baumgarten ◽  
Pascal Knuefermann ◽  
Naoki Nozaki ◽  
Natarajan Sivasubramanian ◽  
Douglas L. Mann ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document