scholarly journals Chloroquine‐treated dendritic cells require STAT1 signaling for their tolerogenic activity

2018 ◽  
Vol 48 (7) ◽  
pp. 1228-1234 ◽  
Author(s):  
Rodolfo Thome ◽  
Amanda Pires Bonfanti ◽  
Javad Rasouli ◽  
Elisabeth Rose Mari ◽  
Guang‐Xian Zhang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Stat1 Signaling ◽  
Tolerogenic Activity

scholarly journals IL-10–Modulated Human Dendritic Cells for Clinical Use: Identification of a Stable and Migratory Subset with Improved Tolerogenic Activity

2016 ◽  
Vol 197 (9) ◽  
pp. 3607-3617 ◽  
Author(s):  
Fanny Kryczanowsky ◽  
Verena Raker ◽  
Edith Graulich ◽  
Matthias P. Domogalla ◽  
Kerstin Steinbrink
Keyword(s):  
Dendritic Cells ◽  
Clinical Use ◽  
Human Dendritic Cells ◽  
Tolerogenic Activity

Contribution of Dehydroepiandrosterone Sulfate and Progesterone to In Vitro Regulation of Tolerogenic Activity of IFN-α-Induced Dendritic Cells

2011 ◽  
Vol 151 (2) ◽  
pp. 205-209
Author(s):  
E. R. Chernykh ◽  
O. Yu. Leplina ◽  
T. V. Tyrinova ◽  
M. A. Tikhonova ◽  
L. V. Sakhno ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dehydroepiandrosterone Sulfate ◽  
Tolerogenic Activity

scholarly journals CD40 signaling augments IL-10 expression and the tolerogenicity of IL-10-induced regulatory dendritic cells

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0248290
Author(s):  
Wojciech Dawicki ◽  
Hui Huang ◽  
Yanna Ma ◽  
Jennifer Town ◽  
Xiaobei Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Wild Type ◽  
Activation Markers ◽  
Asthma Phenotype ◽  
Cell Responses ◽  
Mrna Transfection ◽  
Induced Tolerance ◽  
Tolerogenic Activity

CD40 expressed on stimulatory dendritic cells (DC) provides an important accessory signal for induction of effector T cell responses. It is also expressed at lower levels on regulatory DC (DCreg), but there is little evidence that CD40 signaling contributes to the tolerogenic activity of these cells. Indeed, CD40 silencing within DCreg has been reported to induce T cell tolerance in multiple disease models, suggesting that CD40 is superfluous to DC-induced tolerance. We critically assessed whether CD40 does have a role in tolerance induced by IL-10-differentiated DC (DC10) by using DC10 generating from the bone marrow of wild-type (w.t.) or CD40-/- donor mice, or IL-10-complemented CD40-/- DC10 to treat asthmatic mice. Wild-type DC10 ablated the OVA-asthma phenotype via induction of Foxp3+ Treg responses, but CD40-/- DC10 had no discernible effects on primary facets of the phenotype (e.g., IL-5, IL-9, IL-13 levels, IgE & IgG1 antibodies; p>0.05) and were ≤40% effective in reversal of others. Foxp3+ T cells from the lungs of CD40-/- DC10-treated mice expressed reduced levels of a panel of six Treg-specific activation markers relative to Treg from w.t. DC10-treated mice. Coculture with effector T cells from asthmatic mice induced a marked upregulation of cell surface CD40 on w.t. DC10. While untreated CD40-/- and w.t. DC10 secreted equally low levels of IL-10, stimulation of w.t. DC10 with anti-CD40 for 72 h increased their expression of IL-10 by ≈250%, with no parallel induction of IL-12. Complementing IL-10 expression in CD40-/- DC10 by IL-10 mRNA transfection fully restored the cells’ abilities to suppress the asthma phenotype. In summary, CD40 signaling in DC10 contributes importantly to their expression of IL-10 and to a robust induction of tolerance, including activation of induced Treg.

scholarly journals FC-98 Regulates TLR9-Mediated of CXCL-10 Expression in Dendritic Cells via MAPK and STAT1 Signaling Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Yonghong Yang ◽  
Huan Dou ◽  
Xiaoqin Li ◽  
Yuxian Song ◽  
Wei Gong ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Surface Markers ◽  
Toll Like Receptor ◽  
Cpg Dna ◽  
Bacterial Dna ◽  
Adaptive Immune ◽  
Stat1 Signaling ◽  
And Function ◽  
Antigen Presenting ◽  
Adaptive Immune Systems

Dendritic cells (DCs), as the most potent professional antigen presenting cells, play a crucial role in both innate and adaptive immune systems. Genomic bacterial DNA mimicked by unmethylated CpG motifs is discovered to possess immunostimulatory effects. CpG-DNA recognized by Toll-like receptor 9 (TLR9) on DCs arouses many immune diseases (such as cancer, viral infection, and autoimmune disorders). In this study we investigated the effects of FC-98 on CpG-induced bone marrow-derived DCs (BMDCs). The results showed that FC-98 significantly inhibited the CpG-induced BMDCs maturation and function by suppressing the expression of surface markers (CD40, CD80, CD86, and MHCII). Moreover, FC-98 downregulated the expression of C-X-C motif chemokine 10 (CXCL-10) both at the mRNA and protein level after CpG induction. Meanwhile, FC-98 markedly affected the migration of BMDCs to T cells without affecting their endocytosis capacity. Furthermore, FC-98 was confirmed to decrease CXCL-10 expression by inhibiting CpG-induced activation of MAPKs (ERK, JNK, and p38) and STAT1 signaling. Overall, these results suggested that FC-98 was a potential molecule in the treatment of CXCL-10-mediated immune diseases.

scholarly journals Angiotensin II Regulates Dendritic Cells through Activation of NF-κB /p65, ERK1/2 and STAT1 Pathways

2017 ◽  
Vol 42 (4) ◽  
pp. 1550-1558 ◽  
Author(s):  
Yan Meng ◽  
Chen Chen ◽  
Yang Liu ◽  
Cui Tian ◽  
Hui-Hua Li
Keyword(s):  
Dendritic Cells ◽  
Angiotensin Ii ◽  
Mixed Lymphocyte Culture ◽  
Lymphocyte Culture ◽  
Ang Ii ◽  
Stat1 Signaling ◽  
Underlying Mechanisms ◽  
And Migration ◽  
Dc Maturation

Background: Activation of dendritic cells (DCs) is necessary to initiate immune responses. Angiotensin II (Ang II) has been reported to have a proinflammatory and immunomodulatory function. However, the role of Ang II in regulation of DCs and the underlying mechanisms remain illdefined. Methods: The effects of Ang II on the proliferation, maturation, phagocytosis, migration, and communication with T cells of DCs were analysed utilizing MTT, flow cytometry, ELISA, transwell assay and mixed lymphocyte culture. Results: We found that Ang II treatment significantly inhibited proliferation and phagocytic activity of DCs, but promoted the DC maturation and migration well as the expression of pro-inflammatory cytokines by DCs. In addition, Ang II also stimulated DC-mediated T cell proliferation. These effects were associated with activation of p65/NF-κB, ERK1/2 and STAT1 signaling pathways in DCs. Conclusions: Our results demonstrate that Ang II activates DCs partially through p65/NF-κB, ERK1/2 and STAT1 pathways, and suggest a potential therapeutic target of DC-mediated inflammatory disorders.

Sign in / Sign up

Export Citation Format

Share Document