CC chemokine ligand 2 down-modulation by selected Toll-like receptor agonist combinations contributes to T helper 1 polarization in human dendritic cells

Blood ◽  
2009 ◽  
Vol 114 (4) ◽  
pp. 796-806 ◽  
Author(s):  
Manuela Del Cornò ◽  
Alessandro Michienzi ◽  
Andrea Masotti ◽  
Letizia Da Sacco ◽  
Gian Franco Bottazzo ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Interleukin 12 ◽  
Toll Like Receptor ◽  
T Helper ◽  
Cc Chemokine ◽  
Chemokine Ligand ◽  
Cc Chemokine Ligand 2 ◽  
Chemokine Ligand 2 ◽  
Helper Type

Abstract Toll-like receptor (TLR) signaling activation by pathogens is critical to the induction of immune responses, and demands tight regulation. We describe in this study that CC chemokine ligand 2 (CCL2) secretion triggered by TLR4 or TLR8 engagement is strongly inhibited upon simultaneous activation of both TLRs in human monocyte-derived dendritic cells (DCs). Impaired CCL2 secretion occurs concomitantly to interleukin-12 up-regulation, being part of a complex regulatory circuit ensuring optimal T helper type 1 polarization. Interestingly, triggering selected TLRs or their combinations differently affects nuclear factor-κB p65 activation and microRNA expression. Overall, these results indicate that CCL2 supplies an important immunomodulatory role to DCs, and may contribute to dictate the cytokine profile in T helper type 1 responses induced by DCs.

scholarly journals Selected Toll-like receptor agonist combinations synergistically trigger a T helper type 1–polarizing program in dendritic cells

2005 ◽  
Vol 6 (8) ◽  
pp. 769-776 ◽  
Author(s):  
Giorgio Napolitani ◽  
Andrea Rinaldi ◽  
Francesco Bertoni ◽  
Federica Sallusto ◽  
Antonio Lanzavecchia
Keyword(s):  
Dendritic Cells ◽  
Receptor Agonist ◽  
Toll Like Receptor ◽  
T Helper ◽  
Helper Type

scholarly journals Adenoviruses Activate Human Dendritic Cells without Polarization toward a T-Helper Type 1-Inducing Subset

1999 ◽  
Vol 73 (12) ◽  
pp. 10245-10253 ◽  
Author(s):  
Delphine Rea ◽  
Frederik H. E. Schagen ◽  
Rob C. Hoeben ◽  
Majid Mehtali ◽  
Menzo J. E. Havenga ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Human Monocyte ◽  
Interleukin 12 ◽  
T Helper ◽  
Cell Immunity ◽  
Host Cell Interactions ◽  
Human Dendritic Cells ◽  
Adenovirus Receptor ◽  
Helper Type

ABSTRACT Human monocyte-derived dendritic cells (DC) infected with recombinant adenoviruses (rAd) are promising candidate vaccines for inducing protective immunity against pathogens and tumors. However, since some viruses are known to negatively affect DC function, it is important to investigate the interactions between rAd and DC. We now show that infection by rAd enhances the immunostimulatory capacity of immature human monocyte-derived DC through the upregulation of the costimulatory molecules CD80, CD86, and CD40 and the major histocompatibility complex class I and II molecules. Although rAd infection fails to induce the secretion of interleukin-12 (IL-12) and only marginally induces the expression of the DC maturation marker CD83, it acts in synergy with CD40 triggering in rendering DC fully mature. rAd-infected DC triggered through CD40 produce more IL-12 and are more efficient in eliciting T-helper type 1 responses than DC activated by CD40 triggering only. rAd lacking one or more of the early regions, E1, E2A, E3, and E4, which play an important role in virus-host cell interactions are equally capable of DC activation. Efficient DC infection requires a high multiplicity of infection (>1,000), a fact which can be attributed to the absence of the coxsackievirus and adenovirus receptor on this cell type. Despite the poor ability of DC to be infected by rAd, which may be improved by targeting rAd to alternative DC surface molecules, DC infected with all currently tested rAd constitute potent immunostimulators. Our study provides new insights into the interactions between two highly promising vaccine components, rAd and DC, and indicates that their combination into one vaccine may be very advantageous for the stimulation of T-cell immunity.

scholarly journals Macrophage Migration Inhibitory Factor Induces Macrophage Recruitment via CC Chemokine Ligand 2

2006 ◽  
Vol 177 (11) ◽  
pp. 8072-8079 ◽  
Author(s):  
Julia L. Gregory ◽  
Eric F. Morand ◽  
Sonja J. McKeown ◽  
Jennifer A. Ralph ◽  
Pamela Hall ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Cc Chemokine ◽  
Macrophage Recruitment ◽  
Chemokine Ligand ◽  
Cc Chemokine Ligand 2 ◽  
Chemokine Ligand 2

scholarly journals The prostaglandin E2 receptor EP3 controls CC-chemokine ligand 2–mediated neuropathic pain induced by mechanical nerve damage

2018 ◽  
Vol 293 (25) ◽  
pp. 9685-9695 ◽  
Author(s):  
Elsa-Marie Treutlein ◽  
Katharina Kern ◽  
Andreas Weigert ◽  
Neda Tarighi ◽  
Claus-Dieter Schuh ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Prostaglandin E2 ◽  
Nerve Damage ◽  
Cc Chemokine ◽  
Chemokine Ligand ◽  
Prostaglandin E2 Receptor ◽  
Cc Chemokine Ligand 2 ◽  
Chemokine Ligand 2
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