Local Immune Responses After Skin Vaccination in Neonatal and Adult Pigs With Different Toll-Like-Receptor Agonists as Adjuvant

2020 ◽  
Vol 174 ◽  
pp. 149
Author(s):  
S. Vreman ◽  
J. McCaffrey ◽  
A. Rebel ◽  
A. Moore ◽  
N. Stockhofe-Zurwieden
Keyword(s):  
Immune Responses ◽  
Toll Like Receptor ◽  
Receptor Agonists ◽  
Skin Vaccination

scholarly journals Early immune responses in skin and lymph node after skin delivery of Toll-like receptor agonists in neonatal and adult pigs

Vaccine ◽  
2021 ◽  
Vol 39 (13) ◽  
pp. 1857-1869
Author(s):  
Sandra Vreman ◽  
Johanna M.J. Rebel ◽  
Joanne McCaffrey ◽  
Kristina Ledl ◽  
Ksenia Arkhipova ◽  
...  
Keyword(s):  
Lymph Node ◽  
Immune Responses ◽  
Toll Like Receptor ◽  
Receptor Agonists ◽  
Skin Delivery

scholarly journals Toll-like receptor agonists shape the immune responses to a mannose receptor-targeted cancer vaccine

2014 ◽  
Vol 12 (6) ◽  
pp. 719-728 ◽  
Author(s):  
Li-Zhen He ◽  
Jeffrey Weidlick ◽  
Crystal Sisson ◽  
Henry C Marsh ◽  
Tibor Keler
Keyword(s):  
Immune Responses ◽  
Cancer Vaccine ◽  
Mannose Receptor ◽  
Toll Like Receptor ◽  
Receptor Agonists

Histone deacetylase inhibitors impair innate immune responses to Toll-like receptor agonists and to infection

Blood ◽  
2011 ◽  
Vol 117 (4) ◽  
pp. 1205-1217 ◽  
Author(s):  
Thierry Roger ◽  
Jérôme Lugrin ◽  
Didier Le Roy ◽  
Geneviève Goy ◽  
Matteo Mombelli ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Hdac Inhibitors ◽  
Innate Immune ◽  
Epigenetic Mechanism ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Host Defenses ◽  
Receptor Agonists

Abstract Regulated by histone acetyltransferases and deacetylases (HDACs), histone acetylation is a key epigenetic mechanism controlling chromatin structure, DNA accessibility, and gene expression. HDAC inhibitors induce growth arrest, differentiation, and apoptosis of tumor cells and are used as anticancer agents. Here we describe the effects of HDAC inhibitors on microbial sensing by macrophages and dendritic cells in vitro and host defenses against infection in vivo. HDAC inhibitors down-regulated the expression of numerous host defense genes, including pattern recognition receptors, kinases, transcription regulators, cytokines, chemokines, growth factors, and costimulatory molecules as assessed by genome-wide microarray analyses or innate immune responses of macrophages and dendritic cells stimulated with Toll-like receptor agonists. HDAC inhibitors induced the expression of Mi-2β and enhanced the DNA-binding activity of the Mi-2/NuRD complex that acts as a transcriptional repressor of macrophage cytokine production. In vivo, HDAC inhibitors increased the susceptibility to bacterial and fungal infections but conferred protection against toxic and septic shock. Thus, these data identify an essential role for HDAC inhibitors in the regulation of the expression of innate immune genes and host defenses against microbial pathogens.

scholarly journals Essential role of IRAK-4 protein and its kinase activity in Toll-like receptor–mediated immune responses but not in TCR signaling

2007 ◽  
Vol 204 (5) ◽  
pp. 1013-1024 ◽  
Author(s):  
Tatsukata Kawagoe ◽  
Shintaro Sato ◽  
Andreas Jung ◽  
Masahiro Yamamoto ◽  
Kosuke Matsui ◽  
...  
Keyword(s):  
Immune Responses ◽  
Kinase Activity ◽  
Interleukin 1 ◽  
Cell Receptor ◽  
Nuclear Factor Κb ◽  
Toll Like Receptor ◽  
Tcr Signaling ◽  
Mitogen Activated Protein

Interleukin-1 receptor–associated kinase 4 (IRAK-4) was reported to be essential for the Toll-like receptor (TLR)– and T cell receptor (TCR)–mediated signaling leading to the activation of nuclear factor κB (NF-κB). However, the importance of kinase activity of IRAK family members is unclear. In this study, we investigated the functional role of IRAK-4 activity in vivo by generating mice carrying a knockin mutation (KK213AA) that abrogates its kinase activity. IRAK-4KN/KN mice were highly resistant to TLR-induced shock response. The cytokine production in response to TLR ligands was severely impaired in IRAK-4KN/KN as well as IRAK-4−/− macrophages. The IRAK-4 activity was essential for the activation of signaling pathways leading to mitogen-activated protein kinases. TLR-induced IRAK-4/IRAK-1–dependent and –independent pathways were involved in early induction of NF-κB–regulated genes in response to TLR ligands such as tumor necrosis factor α and IκBζ. In contrast to a previous paper (Suzuki, N., S. Suzuki, D.G. Millar, M. Unno, H. Hara, T. Calzascia, S. Yamasaki, T. Yokosuka, N.J. Chen, A.R. Elford, et al. 2006. Science. 311:1927–1932), the TCR signaling was not impaired in IRAK-4−/− and IRAK-4KN/KN mice. Thus, the kinase activity of IRAK-4 is essential for the regulation of TLR-mediated innate immune responses.

Dose-dependent activation of microglial cells by Toll-like receptor agonists alone and in combination

2005 ◽  
Vol 159 (1-2) ◽  
pp. 87-96 ◽  
Author(s):  
Sandra Ebert ◽  
Joachim Gerber ◽  
Steffi Bader ◽  
Frank Mühlhauser ◽  
Katrin Brechtel ◽  
...  
Keyword(s):  
Microglial Cells ◽  
Toll Like Receptor ◽  
Receptor Agonists ◽  
Dose Dependent
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