scholarly journals Critical role of the Toll-like receptor signal adaptor protein MyD88 in acute allograft rejection

2003 ◽  
Vol 111 (10) ◽  
pp. 1571-1578 ◽  
Author(s):  
Daniel R. Goldstein ◽  
Bethany M. Tesar ◽  
Shizuo Akira ◽  
Fadi G. Lakkis
2010 ◽  
Vol 41 (2) ◽  
pp. 473-484 ◽  
Author(s):  
Emmanuel Letavernier ◽  
Boris Dansou ◽  
Matthias Lochner ◽  
Joëlle Perez ◽  
Agnès Bellocq ◽  
...  

Nature ◽  
2005 ◽  
Vol 439 (7073) ◽  
pp. 208-211 ◽  
Author(s):  
Gagik Oganesyan ◽  
Supriya K. Saha ◽  
Beichu Guo ◽  
Jeannie Q. He ◽  
Arash Shahangian ◽  
...  

2006 ◽  
Vol 45 (6) ◽  
pp. 836-843 ◽  
Author(s):  
Hironori Tsujimoto ◽  
Satoshi Ono ◽  
Atsushi Matsumoto ◽  
Toshinobu Kawabata ◽  
Manabu Kinoshita ◽  
...  

2019 ◽  
Vol 156 (6) ◽  
pp. S-247
Author(s):  
Yun Han Kwon ◽  
Huaqing Wang ◽  
Varun Dewan ◽  
Saad Syed ◽  
Michelle E. Fontes ◽  
...  

2020 ◽  
Vol 21 (10) ◽  
pp. 3681
Author(s):  
Momoko Nakao ◽  
Tomomitsu Miyagaki ◽  
Makoto Sugaya ◽  
Shinichi Sato

Interferon regulatory factors (IRFs) play diverse roles in the regulation of the innate and adaptive immune responses in various diseases. In psoriasis, IRF2 is known to be involved in pathogenesis, while studies on other IRFs are limited. In this study, we investigated the role of IRF5 in psoriasis using imiquimod-induced psoriasis-like dermatitis. Although IRF5 is known to play a critical role in the induction of proinflammatory cytokines by immune cells, such as dendritic cells (DCs), macrophages, and monocytes, IRF5 deficiency unexpectedly exacerbated psoriasiform skin inflammation. The interferon-α and tumor necrosis factor-α mRNA expression levels were decreased, while levels of Th17 cytokines including IL-17, IL-22, and IL-23 were increased in IRF5-deficient mice. Furthermore, IL-23 expression in DCs from IRF5-deficient mice was upregulated both in steady state and after toll-like receptor 7/8 agonist stimulation. Importantly, the expression of IRF4, which is also important for the IL-23 production in DCs, was augmented in DCs from IRF5-deficient mice. Taken together, our results suggest that IRF5 deficiency induces the upregulation of IRF4 in DCs followed by augmented IL-23 production, resulting in the amplification of Th17 responses and the exacerbation of imiquimod-induced psoriasis-like skin inflammation. The regulation of IRF4 or IRF5 expression may be a novel therapeutic approach to psoriasis.


2019 ◽  
Vol 315 ◽  
pp. 23-30 ◽  
Author(s):  
Yun-Jie Shi ◽  
Hai-Feng Gong ◽  
Quan-Quan Zhao ◽  
Xiao-Shuang Liu ◽  
Cong Liu ◽  
...  

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