scholarly journals The effects of toll-like receptor ligand-activated dendritic cells on human CD4⁺T cell responses

2008 ◽  
Author(s):  
Risa Kitawaki Benwell
Keyword(s):  
Dendritic Cells ◽  
Toll Like Receptor ◽  
Receptor Ligand ◽  
Cell Responses

scholarly journals Activation of Dendritic Cells by the Novel Toll-Like Receptor 3 Agonist RGC100

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Kai Naumann ◽  
Rebekka Wehner ◽  
Anett Schwarze ◽  
Christiane Petzold ◽  
Marc Schmitz ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Physicochemical Properties ◽  
Chemical Structure ◽  
Poly I:C ◽  
The Novel ◽  
Toll Like Receptor ◽  
Double Stranded Rna ◽  
Cell Responses ◽  
Vaccination Strategies

Toll-like receptor (TLR) 3 agonists emerged as attractive candidates for vaccination strategies against tumors and pathogens. An important mechanism of action of such agonists is based on the activation of TLR3-expressing dendritic cells (DCs), which display a unique capacity to induce and stimulate T-cell responses. In this context, it has been demonstrated that targeting of TLR3 by double-stranded RNA such as poly(I:C) results in potent activation of DCs. Major disadvantages of poly(I:C) comprise its undefined chemical structure and very poor homogeneity, with subsequent unpredictable pharmacokinetics and high toxicity. In the present study, we evaluated the physicochemical properties and biological activity of the novel TLR3 agonist RGC100. RGC100 has a defined chemical structure, with a defined length (100 bp) and molecular weight (64.9 KDa) and a good solubility. RGC100 is stable in serum and activates myeloid DCs through TLR3 targeting, as evidenced by gene silencing experiments. Activation of mouse and human myeloid CD1c+DCs by RGC100 leads to secretion of several proinflammatory cytokines. In addition, RGC100 improves the ability of CD1c+DCs to stimulate T-cell proliferation. Due to its physicochemical properties and its immunostimulatory properties, RGC100 may represent a promising adjuvant for prophylactic and therapeutic vaccination strategies.

scholarly journals Toll-Like Receptor Ligands Modulate Dendritic Cells to Augment Cytomegalovirus- and HIV-1-Specific T Cell Responses

2003 ◽  
Vol 171 (8) ◽  
pp. 4320-4328 ◽  
Author(s):  
Karin Loré ◽  
Michael R. Betts ◽  
Jason M. Brenchley ◽  
Janaki Kuruppu ◽  
Soorena Khojasteh ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
T Cell Responses ◽  
Toll Like Receptor ◽  
Receptor Ligands ◽  
Cell Responses ◽  
Hiv 1

scholarly journals Expression of the Phosphatase Ppef2 Controls Survival and Function of CD8+ Dendritic Cells

2018 ◽  
Author(s):  
Markus Zwick ◽  
Thomas Ulas ◽  
Yi-Li Cho ◽  
Christine Ried ◽  
Leonie Grosse ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Protein Phosphatase ◽  
Apoptotic Cell ◽  
Model Systems ◽  
Toll Like Receptor ◽  
Cell Responses ◽  
Ef Hands ◽  
And Function ◽  
Dc Maturation

AbstractApoptotic cell death of Dendritic cells (DCs) is critical for immune homeostasis. Although intrinsic mechanisms controlling DC death have not been fully characterized up to now, experimentally enforced inhibition of DC-death causes various autoimmune diseases in model systems. We have generated mice deficient for Protein Phosphatase with EF-Hands 2 (Ppef2), which is selectively expressed in CD8+ DCs, but not in other related DC subtypes such as tissue CD103+ DCs. Ppef2 is down-regulated rapidly upon maturation of DCs by toll-like receptor stimuli, but not upon triggering of CD40. Ppef2-deficient CD8+ DCs accumulate the pro-apoptotic Bcl-2-like protein 11 (Bim) and show increased apoptosis and reduced competitve repopulation capacities. Furthermore, Ppef2−/−CD8+ DCs have strongly diminished antigen presentation capacities in vivo, as CD8+ T cells primed by Ppef2−/− CD8+ DCs undergo reduced expansion. In conclusion, our data suggests that Ppef2 is crucial to support survival of immature CD8+ DCs, while Ppef2 down-regulation during DC-maturation limits T cell responses.

scholarly journals Distinct Uptake Mechanisms but Similar Intracellular Processing of Two Different Toll-like Receptor Ligand-Peptide Conjugates in Dendritic Cells

2007 ◽  
Vol 282 (29) ◽  
pp. 21145-21159 ◽  
Author(s):  
Selina Khan ◽  
Martijn S. Bijker ◽  
Jimmy J. Weterings ◽  
Hans J. Tanke ◽  
Gosse J. Adema ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Toll Like Receptor ◽  
Peptide Conjugates ◽  
Receptor Ligand ◽  
Intracellular Processing ◽  
Uptake Mechanisms

scholarly journals CD73+ Dendritic Cells in Cascading Th17 Responses of Experimental Autoimmune Uveitis-Induced Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
MinHee K. Ko ◽  
Hui Shao ◽  
Henry J. Kaplan ◽  
Deming Sun
Keyword(s):  
Dendritic Cells ◽  
Critical Role ◽  
Γδ T Cells ◽  
Adenosine Monophosphate ◽  
Toll Like Receptor ◽  
Promoting Effect ◽  
Receptor Ligand ◽  
Antigen Presenting ◽  
Different Levels ◽  
Experimental Autoimmune

Previous studies have shown that CD73 is pivotal in the conversion of pro-inflammatory adenosine triphosphate into anti-inflammatory adenosine and that immune cells of the same type that express different levels of CD73 are functionally distinct. In this study we show that adenosine enhances the Th17 promoting effect of dendritic cells (DCs), and DCs expressing CD73 critically augment Th17 responses. Bone marrow dendritic cells (BMDCs) do not constantly express CD73; however, a significant portion of the BMDCs expressed CD73 after exposure to Toll-like receptor ligand, leading to stronger Th17 responses by converting adenosine monophosphate to adenosine. We show that the CD73+ BMDCs play a critical role in cascading Th17 responses, and CD73+ BMDCs are functionally augmented after treatment with Toll-like receptor ligand. Splenic antigen presenting cells (DCs) of CD73−/− mouse have a poor Th17-stimulating effect, even after exposure to lipopolysaccharide (LPS) or γδ T cells, indicating that induction of CD73+ DCs is critically involved in augmented Th17 responses. We conclude that CD73+ DCs critically trigger cascading Th17 responses, and the activated Th17 cells that express CD73 further augment Th17 responses, leading to cascading exacerbation. Hence, disabling the CD73 function of DCs should block this cascading response and mitigate Th17 responses.

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