A critical role of CpG motifs in a murine peritonitis model by their binding to highly expressed toll-like receptor-9 on liver NKT cells

2006 ◽  
Vol 45 (6) ◽  
pp. 836-843 ◽  
Author(s):  
Hironori Tsujimoto ◽  
Satoshi Ono ◽  
Atsushi Matsumoto ◽  
Toshinobu Kawabata ◽  
Manabu Kinoshita ◽  
...  
Keyword(s):  
Critical Role ◽  
Nkt Cells ◽  
Toll Like Receptor ◽  
Cpg Motifs ◽  
Peritonitis Model

Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response

Nature ◽  
2005 ◽  
Vol 439 (7073) ◽  
pp. 208-211 ◽  
Author(s):  
Gagik Oganesyan ◽  
Supriya K. Saha ◽  
Beichu Guo ◽  
Jeannie Q. He ◽  
Arash Shahangian ◽  
...  
Keyword(s):  
Critical Role ◽  
Antiviral Response ◽  
Toll Like Receptor

1153 – Critical Role of Toll-Like Receptor 2 in Mediating Serotonin Production in Gut

2019 ◽  
Vol 156 (6) ◽  
pp. S-247
Author(s):  
Yun Han Kwon ◽  
Huaqing Wang ◽  
Varun Dewan ◽  
Saad Syed ◽  
Michelle E. Fontes ◽  
...  
Keyword(s):  
Critical Role ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Exacerbated Imiquimod-Induced Psoriasis-Like Skin Inflammation in IRF5-Deficient Mice

2020 ◽  
Vol 21 (10) ◽  
pp. 3681
Author(s):  
Momoko Nakao ◽  
Tomomitsu Miyagaki ◽  
Makoto Sugaya ◽  
Shinichi Sato
Keyword(s):  
Critical Role ◽  
Skin Inflammation ◽  
Interferon Α ◽  
Toll Like Receptor ◽  
Adaptive Immune ◽  
Th17 Cytokines ◽  
Factor Α ◽  
Deficient Mice ◽  
Necrosis Factor

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.

Critical role of toll-like receptor 4 (TLR4) in dextran sulfate sodium (DSS)-Induced intestinal injury and repair

2019 ◽  
Vol 315 ◽  
pp. 23-30 ◽  
Author(s):  
Yun-Jie Shi ◽  
Hai-Feng Gong ◽  
Quan-Quan Zhao ◽  
Xiao-Shuang Liu ◽  
Cong Liu ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Critical Role ◽  
Intestinal Injury ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Injury And Repair

scholarly journals A critical role for IRAK4 kinase activity in Toll-like receptor–mediated innate immunity

2007 ◽  
Vol 204 (5) ◽  
pp. 1025-1036 ◽  
Author(s):  
Tae Whan Kim ◽  
Kirk Staschke ◽  
Katarzyna Bulek ◽  
Jianhong Yao ◽  
Kristi Peters ◽  
...  
Keyword(s):  
Immune Responses ◽  
Kinase Activity ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Type I ◽  
Toll Like Receptor ◽  
Chemokine Production ◽  
Cytokines And Chemokines ◽  
Plasmacytoid Dcs

IRAK4 is a member of IL-1 receptor (IL-1R)–associated kinase (IRAK) family and has been shown to play an essential role in Toll-like receptor (TLR)–mediated signaling. We recently generated IRAK4 kinase-inactive knock-in mice to examine the role of kinase activity of IRAK4 in TLR-mediated signaling pathways. The IRAK4 kinase–inactive knock-in mice were completely resistant to lipopolysaccharide (LPS)- and CpG-induced shock, due to impaired TLR-mediated induction of proinflammatory cytokines and chemokines. Although inactivation of IRAK4 kinase activity did not affect the levels of TLR/IL-1R–mediated nuclear factor κB activation, a reduction of LPS-, R848-, and IL-1–mediated mRNA stability contributed to the reduced cytokine and chemokine production in bone marrow–derived macrophages from IRAK4 kinase–inactive knock-in mice. Both TLR7- and TLR9-mediated type I interferon production was abolished in plasmacytoid dendritic cells isolated from IRAK4 knock-in mice. In addition, influenza virus–induced production of interferons in plasmacytoid DCs was also dependent on IRAK4 kinase activity. Collectively, our results indicate that IRAK4 kinase activity plays a critical role in TLR-dependent immune responses.

Sign in / Sign up

Export Citation Format

Share Document