scholarly journals The TIR ‐domain‐containing adapter inducing interferon‐β‐dependent signaling cascade plays a crucial role in ischemia–reperfusion‐induced retinal injury, whereas the contribution of the myeloid differentiation primary response 88‐dependent signaling cascade is not as pivotal

2014 ◽  
Vol 40 (3) ◽  
pp. 2502-2512 ◽  
Author(s):  
Galina Dvoriantchikova ◽  
Andrea Rachelle C. Santos ◽  
Dagmara Danek ◽  
Xenia Dvoriantchikova ◽  
Dmitry Ivanov
Life Sciences ◽  
2016 ◽  
Vol 162 ◽  
pp. 33-40 ◽  
Author(s):  
Anyelo Duran ◽  
Nereida Valero ◽  
Jesus Mosquera ◽  
Lineth Delgado ◽  
Melchor Alvarez-Mon ◽  
...  

2015 ◽  
Vol 7 (6) ◽  
pp. 637-646 ◽  
Author(s):  
Miriam H.P. van Lieshout ◽  
Sandrine Florquin ◽  
Cornelis vanʼt Veer ◽  
Alex F. de Vos ◽  
Tom van der Poll

Klebsiella pneumoniae is an important cause of Gram-negative pneumonia and sepsis. Mice deficient for TIR-domain-containing adaptor-inducing interferon-β (TRIF) demonstrate enhanced bacterial growth and dissemination during Klebsiella pneumonia. We show here that the impaired antibacterial defense of TRIF mutant mice is associated with absent interferon (IFN)-γ production in the lungs. IFN-γ production by splenocytes in response to K. pneumoniae in vitro was critically dependent on Toll-like receptor 4 (TLR4), the common TLR adaptor myeloid differentiation primary response gene (MyD88) and TRIF. Reconstitution of TRIF mutant mice with recombinant IFN-γ via the airways reduced bacterial loads in lungs and distant body sites to levels measured in wild-type mice, and partially restored pulmonary cytokine levels. The IFN-γ-induced, improved, enhanced antibacterial response in TRIF mutant mice occurred at the expense of increased hepatocellular injury. These data indicate that TRIF mediates antibacterial defense during Gram-negative pneumonia, at least in part, by inducing IFN-γ at the primary site of infection.


2021 ◽  
pp. 175342592110513
Author(s):  
F. Linzee Mabrey ◽  
Eric D Morrell ◽  
Mark M Wurfel

COVID-19 is both a viral illness and a disease of immunopathology. Proximal events within the innate immune system drive the balance between deleterious inflammation and viral clearance. We hypothesize that a divergence between the generation of excessive inflammation through over activation of the TLR associated myeloid differentiation primary response (MyD88) pathway relative to the TIR-domain-containing adaptor-inducing IFN-β (TRIF) pathway plays a key role in COVID-19 severity. Both viral elements and damage associated host molecules act as TLR ligands in this process. In this review, we detail the mechanism for this imbalance in COVID-19 based on available evidence, and we discuss how modulation of critical elements may be important in reducing severity of disease.


2010 ◽  
Vol 126 (1) ◽  
pp. 172-175 ◽  
Author(s):  
Daniel H. Conway ◽  
Jasmeen Dara ◽  
Asen Bagashev ◽  
Kathleen E. Sullivan

2011 ◽  
Vol 52 (10) ◽  
pp. 7187 ◽  
Author(s):  
Galina Dvoriantchikova ◽  
Eleut Hernandez ◽  
Jeff Grant ◽  
Andrea Rachelle C. Santos ◽  
Huan Yang ◽  
...  

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