scholarly journals Myeloid Differentiation Primary Response Gene (88)– and Toll‐Like Receptor 2–Deficient Mice Are Susceptible to Infection with AerosolizedLegionella pneumophila

2006 ◽  
Vol 193 (12) ◽  
pp. 1693-1702 ◽  
Author(s):  
Thomas R. Hawn ◽  
Kelly D. Smith ◽  
Alan Aderem ◽  
Shawn J. Skerrett
Keyword(s):  
Primary Response ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Response Gene ◽  
Primary Response Gene ◽  
Toll Like Receptor 2 ◽  
Deficient Mice

scholarly journals Kaposi's Sarcoma-Associated Herpesvirus Reduces Cellular Myeloid Differentiation Primary-Response Gene 88 (MyD88) Expression via Modulation of Its RNA

2015 ◽  
Vol 90 (1) ◽  
pp. 180-188 ◽  
Author(s):  
Amy Lingel ◽  
Erica Ehlers ◽  
Qianli Wang ◽  
Mingxia Cao ◽  
Charles Wood ◽  
...  
Keyword(s):  
Kaposi's Sarcoma ◽  
Rna Synthesis ◽  
Kaposi’S Sarcoma ◽  
Primary Response ◽  
Lytic Replication ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Transcription Activator ◽  
Response Gene ◽  
Primary Response Gene

ABSTRACTKaposi's sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignancies. The replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. Interleukin 1 (IL-1) is a major mediator for inflammation and plays an important role in both innate and adaptive immunity. Myeloid differentiation primary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like receptor signaling. In this study, we identified a novel mechanism by which KSHV interferes with host inflammation and immunity. KSHV RTA specifically reduces the steady-state protein levels of MyD88, and physiological levels of MyD88 are downregulated during KSHV lytic replication when RTA is expressed. The N-terminal region of RTA is required for the reduction of MyD88. Additional studies demonstrated that RTA targets MyD88 expression at the RNA level, inhibits RNA synthesis of MyD88, and may bind MyD88 RNA. Finally, RTA inhibits IL-1-mediated activation of NF-κB. Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this work may expand our understanding of how KSHV evades host inflammation and immunity for its survivalin vivo.IMPORTANCEMyD88 is an important molecule for IL-1-mediated inflammation and Toll-like receptor (TLR) signaling. This work shows that KSHV inhibits MyD88 expression through a novel mechanism. KSHV RTA may bind to MyD88 RNA, suppresses RNA synthesis of MyD88, and inhibits IL-1-mediated signaling. This work may expand our understanding of how KSHV evades host inflammation and immunity.

scholarly journals Identification of Binding Sites for Myeloid Differentiation Primary Response Gene 88 (MyD88) and Toll-like Receptor 4 in MyD88 Adapter-like (Mal)

2013 ◽  
Vol 288 (17) ◽  
pp. 12054-12066 ◽  
Author(s):  
Celia Bovijn ◽  
Anne-Sophie Desmet ◽  
Isabel Uyttendaele ◽  
Tim Van Acker ◽  
Jan Tavernier ◽  
...  
Keyword(s):  
Binding Sites ◽  
Primary Response ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Response Gene ◽  
Primary Response Gene

scholarly journals Nucleoredoxin Negatively Regulates Toll-like Receptor 4 Signaling via Recruitment of Flightless-I to Myeloid Differentiation Primary Response Gene (88)

2010 ◽  
Vol 285 (24) ◽  
pp. 18586-18593 ◽  
Author(s):  
Tatsuya Hayashi ◽  
Yosuke Funato ◽  
Takeshi Terabayashi ◽  
Akifumi Morinaka ◽  
Reiko Sakamoto ◽  
...  
Keyword(s):  
Primary Response ◽  
Myeloid Differentiation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Response Gene ◽  
Primary Response Gene
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