scholarly journals Subsets of Human Dendritic Cell Precursors Express Different Toll-like Receptors and Respond to Different Microbial Antigens

2001 ◽  
Vol 194 (6) ◽  
pp. 863-870 ◽  
Author(s):  
Norimitsu Kadowaki ◽  
Stephen Ho ◽  
Svetlana Antonenko ◽  
Rene de Waal Malefyt ◽  
Robert A. Kastelein ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Expression Profiles ◽  
Lipoteichoic Acid ◽  
Poly I:C ◽  
Human Dendritic Cell ◽  
Toll Like Receptors ◽  
Double Stranded Rna ◽  
Tlr9 Ligand ◽  
Tnf Α ◽  
Necrosis Factor

Toll-like receptors (TLRs) are ancient microbial pattern recognition receptors highly conserved from Drosophila to humans. To investigate if subsets of human dendritic cell precursors (pre-DC), including monocytes (pre-DC1), plasmacytoid DC precursors (pre-DC2), and CD11c+ immature DCs (imDCs) are developed to recognize different microbes or microbial antigens, we studied their TLR expression and responses to microbial antigens. We demonstrate that whereas monocytes preferentially express TLR 1, 2, 4, 5, and 8, plasmacytoid pre-DC strongly express TLR 7 and 9. In accordance with these TLR expression profiles, monocytes respond to the known microbial ligands for TLR2 (peptidoglycan [PGN], lipoteichoic acid) and TLR4 (lipopolysaccharide), by producing tumor necrosis factor (TNF)-α and interleukin (IL)-6. In contrast, plasmacytoid pre-DCs only respond to the microbial TLR9-ligand, CpG-ODNs (oligodeoxynucleotides [ODNs] containing unmethylated CpG motifs), by producing IFN-α. CD11c+ imDCs preferentially express TLR 1, 2, and 3 and respond to TLR 2-ligand PGN by producing large amounts of TNF-α, and to viral double-stranded RNA-like molecule poly I:C, by producing IFN-α and IL-12. The expression of distinct sets of TLRs and the corresponding difference in reactivity to microbial molecules among subsets of pre-DCs and imDCs support the concept that they have developed through distinct evolutionary pathways to recognize different microbial antigens.

The Augmented Productions of Neopterin and Cytokines from Macrophages/monocytes in vitro

Pteridines ◽  
1996 ◽  
Vol 7 (3) ◽  
pp. 72-76
Author(s):  
Tadashi Lizuka ◽  
Mitsuyo Sasaki ◽  
Hitomi Kamisako ◽  
Ko Oishi ◽  
Shigeru Uemura ◽  
...  
Keyword(s):  
Kawasaki Disease ◽  
Interleukin 1 ◽  
Poly I:C ◽  
Recombinant Interferon ◽  
Preliminary Examination ◽  
Tnf Α ◽  
Ifn Γ ◽  
Factor Α ◽  
Necrosis Factor

Summary In Kawasaki disease patients, increases in excretion of urinary neopterin coincided with fever and monocytosis in peripheral blood. We examined the products of neopterin, tumor necrosis factor-α (TNFα) and Interleukin-1 β (1L-1β) from healthy adult macrophages/monocytes (Mφ>/M), after stimulation with several activators to obtain some understanding of Kawasaki disease. Upon stimulation with either lipopolysaccharide (LPS) or polyinosinate-polycytidylate (Poly I:C), the Mφ/M released neopterin and pyogenic products (TNF-α or 1L-1β). The release of neopterin was eliminated by the addition of the anti-interferon-y antibody. The production of both TNF-α, 1L-1β and neopterin from Mφ/M upon stimulation of LPS was augmented in a co-culture with low dose recombinant interferon-y (rIFN-γ). Upon stimulation with rIFN-γ alone, however, the Mφ/M released neopterin but not the pyogenic products. A preliminary examination failed to detect. any difference in the response of the Mφ/M in adults annd children after stimulation with LPS. We concluded that some endotoxins could trigger the onset of Kawasaki disease and that endogenous IFN-γ can play an important role in the abnormality of Kawasaki disease patients

The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism

2004 ◽  
Vol 287 (4) ◽  
pp. R759-R766 ◽  
Author(s):  
Marie-Eve Fortier ◽  
Stephen Kent ◽  
Helen Ashdown ◽  
Stephen Poole ◽  
Patricia Boksa ◽  
...  
Keyword(s):  
Body Temperature ◽  
Viral Infections ◽  
Interleukin 1 ◽  
Male Rats ◽  
Poly I:C ◽  
Polyinosinic:Polycytidylic Acid ◽  
Tnf Α ◽  
Necrosis Factor ◽  
Dependent Mechanism

Polyinosinic:polycytidylic acid (poly I:C) is a synthetic double-stranded RNA that is used experimentally to model viral infections in vivo. Previous studies investigating the inflammatory properties of this agent in rodents demonstrated that it is a potent pyrogen. However, the mechanisms underlying this response have not been fully elucidated. In the current study, we examined the effects of peripheral administration of poly I:C on body temperature and cytokine production. Male rats were implanted with biotelemetry devices and randomly assigned to one of the following three groups: poly I:C + saline, poly I:C + interleukin-1 receptor antagonist (IL-1ra), or saline + saline. Maximal fever of 1.6°C above baseline was observed 3 h after an intraperitoneal injection of poly I:C (750 μg/kg). Pretreatment with IL-1ra diminished this response by >50% (maximum body temperature = 0.6°C above baseline). Plasma IL-6 concentration increased fivefold 2 h post-poly I:C compared with saline-injected rats; levels returned to baseline 4 h postinjection. Pretreatment with IL-1ra prevented this rise in IL-6. Plasma tumor necrosis factor (TNF)-α was also increased more than fourfold 2 h postinjection but remained unaffected by IL-1ra treatment. IL-1β and cyclooxygenase-2 mRNA were significantly upregulated in the hypothalamus of poly I:C-treated animals. Finally, poly I:C decreased food intake by 30%, but this response was not altered by pretreatment with IL-1ra. These results suggest that poly I:C induces fever, but not anorexia, through an IL-1 and prostaglandin-dependent mechanism.

scholarly journals Allergen-Specific Immunotherapy Alters the Frequency, as well as the FcR and CLR Expression Profiles of Human Dendritic Cell Subsets

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148838 ◽  
Author(s):  
Kristina Lundberg ◽  
Frida Rydnert ◽  
Sissela Broos ◽  
Morgan Andersson ◽  
Lennart Greiff ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Specific Immunotherapy ◽  
Expression Profiles ◽  
Human Dendritic Cell ◽  
Allergen Specific Immunotherapy ◽  
Dendritic Cell Subsets

Cycling of human dendritic cell effector phenotypes in response to TNF‐α: modification of the current ‘maturation’ paradigm and implications for in vivo immunoregulation

1999 ◽  
Vol 13 (14) ◽  
pp. 2021-2030 ◽  
Author(s):  
Edward L. Nelson ◽  
Susan Strobl ◽  
Jeff Subleski ◽  
Darue Prieto ◽  
William C. Kopp ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Human Dendritic Cell ◽  
Tnf Α ◽  
Cell Effector

scholarly journals Regulation of STAT pathways and IRF1 during human dendritic cell maturation by TNF-α and PGE2

2008 ◽  
Vol 84 (5) ◽  
pp. 1353-1360 ◽  
Author(s):  
Yang Hu ◽  
Kyung-Hyun Park-Min ◽  
Anna Yarilina ◽  
Lionel B. Ivashkiv
Keyword(s):  
Dendritic Cell ◽  
Dendritic Cell Maturation ◽  
Cell Maturation ◽  
Human Dendritic Cell ◽  
Tnf Α

scholarly journals Peptidoglycan and Lipoteichoic Acid from Staphylococcus aureus Induce Tumor Necrosis Factor Alpha, Interleukin 6 (IL-6), and IL-10 Production in Both T Cells and Monocytes in a Human Whole Blood Model

2000 ◽  
Vol 68 (7) ◽  
pp. 3965-3970 ◽  
Author(s):  
J. E. Wang ◽  
P. F. Jørgensen ◽  
M. Almlöf ◽  
C. Thiemermann ◽  
S. J. Foster ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Lipoteichoic Acid ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT We have examined the ability of peptidoglycan (PepG) and lipoteichoic acid (LTA) isolated from Staphylococcus aureusto induce the release of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-10 in whole human blood and identified the cellular origins of these cytokines. Both PepG and LTA induced transient increases in TNF-α and IL-10 in plasma, with peak values at 6 and 12 h, respectively. IL-6 values increased throughout the experimental period (24 h). The TNF-α, IL-6, and IL-10 release induced by PepG and LTA was dose dependent. Only PepG was a potent inducer of TNF-α secretion. After stimulation of whole blood with PepG or LTA, very pure populations of monocytes (CD14 positive), T cells (CD2 positive), B cells (CD19 positive), and granulocytes (CD15 positive) were isolated by immunomagnetic separation and analyzed by reverse transcription-PCR for mRNA transcripts encoding TNF-α, IL-6, and IL-10. The TNF-α mRNA results were inconclusive. In contrast, PepG induced IL-6 and IL-10 mRNA accumulation in both T cells and monocytes. LTA, as well as lipopolysaccharide, induced IL-6 and IL-10 mRNA production in monocytes and possibly in T cells. Whether granulocytes and B cells produce cytokines in response to bacterial stimuli remains obscure. Blockade of the CD14 receptors with monoclonal antibodies (18D11) had no influence on the PepG-induced release of TNF-α but attenuated the LTA-induced release of the same cytokine. In conclusion, our data indicate that circulating T cells and monocytes contribute to cytokine production in sepsis caused by gram-positive bacteria.

Activation of natural killer cells inhibits liver regeneration in toxin-induced liver injury model in mice via a tumor necrosis factor-α-dependent mechanism

2010 ◽  
Vol 299 (1) ◽  
pp. G275-G282 ◽  
Author(s):  
Hairong Wei ◽  
Haiming Wei ◽  
Hua Wang ◽  
Zhigang Tian ◽  
Rui Sun
Keyword(s):  
Liver Injury ◽  
Liver Regeneration ◽  
Nk Cells ◽  
Tumor Necrosis ◽  
Nk Cell ◽  
Poly I:C ◽  
Injury Model ◽  
Tnf Α ◽  
Ifn Γ ◽  
Necrosis Factor

Liver lymphocytes are enriched in natural killer (NK) cells, and activation of NK cells by injection of polyinosinic-polycytidylic acid (poly I:C) inhibits liver regeneration in the partial hepatectomy model via production of IFN-γ. However, the role of NK cells in liver regeneration in a model of carbon tetrachloride (CCl4)-induced liver injury remains unknown. In this study, we investigated the effect of activation of NK cells induced by poly I:C on liver regeneration in the CCl4 model. Administration of poly I:C suppressed liver regeneration in CCl4-treated mice. Depletion of NK cells but not Kupffer cells or T cells restored liver regeneration in poly I:C/CCl4-treated mice. Poly I:C and CCl4 cotreatment synergistically induced accumulation of NK cells in the liver and NK cell production of IFN-γ and tumor necrosis factor (TNF)-α. Serum levels of these two cytokines were also synergistically induced after poly I:C and CCl4 treatment. Finally, blockage of TNF-α but not IFN-γ restored liver regeneration in poly I:C/CCl4-treated mice. Taken together, these findings suggest that poly I:C treatment inhibits liver regeneration in the CCl4-induced liver injury model via induction of NK cell production of TNF-α.

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