scholarly journals ER stress and its regulator X-box-binding protein-1 enhance polyIC-induced innate immune response in dendritic cells

2011 ◽  
Vol 41 (4) ◽  
pp. 1086-1097 ◽  
Author(s):  
Fanlei Hu ◽  
Xiaofei Yu ◽  
Hongxia Wang ◽  
Daming Zuo ◽  
Chunqing Guo ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Er Stress ◽  
Innate Immune Response ◽  
Binding Protein ◽  
Innate Immune

scholarly journals Salmonella escapes adaptive immune response via SIRT2 mediated modulation of innate immune response in dendritic cells

2018 ◽  
Vol 14 (11) ◽  
pp. e1007437 ◽  
Author(s):  
Mayuri Gogoi ◽  
Kasturi Chandra ◽  
Mohsen Sarikhani ◽  
Ramya Ramani ◽  
Nagalingam Ravi Sundaresan ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Adaptive Immune

scholarly journals Correction: Salmonella escapes adaptive immune response via SIRT2 mediated modulation of innate immune response in dendritic cells

2020 ◽  
Vol 16 (2) ◽  
pp. e1008345
Author(s):  
Mayuri Gogoi ◽  
Kasturi Chandra ◽  
Mohsen Sarikhani ◽  
Ramya Ramani ◽  
Nagalingam Ravi Sundaresan ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Adaptive Immune

The Regulatory Role of Dendritic Cells in the Innate Immune Response

2014 ◽  
pp. 95-109 ◽  
Author(s):  
F. Granucci ◽  
S. Feau ◽  
I. Zanoni ◽  
G. Raimondi ◽  
N. Pavelka ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Regulatory Role

scholarly journals The Autophagy Protein ATG16L1 Is Required for Sindbis Virus-Induced eIF2α Phosphorylation and Stress Granule Formation

Viruses ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 39
Author(s):  
Matthew Jefferson ◽  
Benjamin Bone ◽  
Jasmine L. Buck ◽  
Penny P. Powell
Keyword(s):  
Immune Response ◽  
Protein Synthesis ◽  
Innate Immune Response ◽  
Viral Protein ◽  
Sindbis Virus ◽  
Binding Protein ◽  
Innate Immune ◽  
Stress Granule ◽  
Viral Protein Synthesis ◽  
Eif2α Phosphorylation

Sindbis virus (SINV) infection induces eIF2α phosphorylation, which leads to stress granule (SG) assembly. SINV infection also stimulates autophagy, which has an important role in controlling the innate immune response. The importance of autophagy to virus-induced translation arrest is not well understood. In this study, we show that the autophagy protein ATG16L1 not only regulates eIF2α phosphorylation and the translation of viral and antiviral proteins, but also controls SG assembly. Early in infection (2hpi), capsids were recruited by host factors Cytotoxic Granule-Associated RNA Binding Protein (TIA1), Y-box binding protein 1 (YBX1), and vasolin-containing protein 1 (VCP), to a single perinuclear body, which co-localized with the viral pattern recognition sensors, double stranded RNA-activated protein-kinase R (PKR) and RIG-I. By 6hpi, there was increased eIF2α phosphorylation and viral protein synthesis. However, in cells lacking the autophagy protein ATG16L1, SG assembly was inhibited and capsid remained in numerous small foci in the cytoplasm containing YBX1, TIA1 with RIG-I, and these persisted for over 8hpi. In the absence of ATG16L1, there was little phosphorylation of eIF2α and low levels of viral protein synthesis. Compared to wild type cells, there was potentiated interferon protein and interferon-stimulated gene (ISG) mRNA expression. These results show that ATG16L1 is required for maximum eIF2α phosphorylation, proper SG assembly into a single perinuclear focus, and for attenuating the innate immune response. Therefore, this study shows that, in the case of SINV, ATG16L1 is pro-viral, required for SG assembly and virus replication.

scholarly journals Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Aleksandra Kezić ◽  
Natasa Stajic ◽  
Friedrich Thaiss
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Reperfusion Injury ◽  
Innate Immune Response ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Graft Function ◽  
Innate Immune ◽  
Injury Potential ◽  
Kidney Ischemia

Acute kidney injury caused by ischemia and subsequent reperfusion is associated with a high rate of mortality and morbidity. Ischemia/reperfusion injury in kidney transplantation causes delayed graft function and is associated with more frequent episodes of acute rejection and progression to chronic allograft nephropathy. Alloantigen-independent inflammation is an important process, participating in pathogenesis of injurious response, caused by ischemia and reperfusion. This innate immune response is characterized by the activity of classical cells belonging to the immune system, such as neutrophils, macrophages, dendritic cells, lymphocytes, and also tubular epithelial cells and endothelial cells. These immune cells not only participate in inflammation after ischemia exerting detrimental influence but also play a protective role in the healing response from ischemia/reperfusion injury. Delineating of complex mechanisms of their actions could be fruitful in future prevention and treatment of ischemia/reperfusion injury. Among numerous so far conducted experiments, observed immunomodulatory role of adenosine and adenosine receptor agonists in complex interactions of dendritic cells, natural killer T cells, and T regulatory cells is emphasized as promising in the treatment of kidney ischemia/reperfusion injury. Potential pharmacological approaches which decrease NF-κB activity and antagonize mechanisms downstream of activated Toll-like receptors are discussed.

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