Immunomodulatory property and its regulatory mechanism of double network hydrogel on dendritic cells

Author(s):  
Fujun Zhu ◽  
Yalin Tong ◽  
Yao Wu ◽  
Ning Dong ◽  
Zhiyong Sheng ◽  
...  
Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 583
Author(s):  
Ze-Jun Yang ◽  
Bo-Ya Wang ◽  
Tian-Tian Wang ◽  
Fei-Fei Wang ◽  
Yue-Xin Guo ◽  
...  

Dendritic cells (DCs), including conventional DCs (cDCs) and plasmacytoid DCs (pDCs), serve as the sentinel cells of the immune system and are responsible for presenting antigen information. Moreover, the role of DCs derived from monocytes (moDCs) in the development of inflammation has been emphasized. Several studies have shown that the function of DCs can be influenced by gut microbes including gut bacteria and viruses. Abnormal changes/reactions in intestinal DCs are potentially associated with diseases such as inflammatory bowel disease (IBD) and intestinal tumors, allowing DCs to be a new target for the treatment of these diseases. In this review, we summarized the physiological functions of DCs in the intestinal micro-environment, their regulatory relationship with intestinal microorganisms and their regulatory mechanism in intestinal diseases.


2010 ◽  
Vol 33 (1) ◽  
pp. 40-52 ◽  
Author(s):  
Michael W. Traxlmayr ◽  
Daniela Wesch ◽  
Alexander M. Dohnal ◽  
Philipp Funovics ◽  
Michael B. Fischer ◽  
...  

2004 ◽  
Vol 199 (4) ◽  
pp. 525-533 ◽  
Author(s):  
Ikuo Shiratori ◽  
Kouetsu Ogasawara ◽  
Takashi Saito ◽  
Lewis L. Lanier ◽  
Hisashi Arase

Paired receptors that consist of highly related activating and inhibitory receptors are widely involved in the regulation of the immune system. Here, we report a mouse orthologue of the human activating paired immunoglobulin-like type 2 receptor (PILR) β, which was cloned from a cDNA library of natural killer (NK) cells based on its ability to associate with the DAP12 signaling adaptor protein. The activating PILRβ was expressed not only on NK cells but also on dendritic cells and macrophages. Furthermore, we have identified a novel CD99-like molecule as a ligand for the activating PILRβ and inhibitory PILRα receptors. Transcripts of PILR ligand are present in many tissues, including some T cell lines. Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRβ. Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.


2012 ◽  
Vol 188 (12) ◽  
pp. 5898-5905 ◽  
Author(s):  
Antonia L. Pritchard ◽  
Melanie L. Carroll ◽  
Julie G. Burel ◽  
Olivia J. White ◽  
Simon Phipps ◽  
...  

2021 ◽  
Vol 10 (23) ◽  
pp. 5610
Author(s):  
Tomoyo Matsuda-Taniguchi ◽  
Masaki Takemura ◽  
Takeshi Nakahara ◽  
Akiko Hashimoto-Hachiya ◽  
Ayako Takai-Yumine ◽  
...  

Psoriasis is a chronic inflammatory skin disease, and its immune mechanism has been profoundly elucidated. Biologics targeting interleukin (IL)-23 have prevented the development of psoriasis. As major sources of IL-23, dendritic cells (DCs) play a pivotal role in psoriasis; however, the regulatory mechanism of IL-23 in DCs remains unclear. IL-36γ was reported to reflect the disease activity of psoriasis. Therefore, we hypothesized that IL-36γ may affect IL-23 production in DCs. To reveal the mechanism by which IL-36γ controls IL-23 production in DCs, we analyzed murine bone marrow-derived DCs (BMDCs) stimulated with IL-36γ. IL-36γ stimulation upregulated the mRNA and protein expression of Nfkbiz in BMDCs. Nfkbiz knockdown using siRNA transfection partially inhibited the upregulation of IL-23 mRNA expression induced by IL-36γ stimulation. Since NF-κB signaling regulates Nfkbiz expression and the anti-diabetic agent metformin reportedly modulates NF-κB signaling, we examined the effect of metformin treatment on IL-36γ-induced IL-23 production. Metformin treatment impaired the phosphorylation of NF-κB induced by IL-36γ stimulation with the subsequent downregulation of Nfkbiz, resulting in the inhibition of IL-23 production in BMDCs. These data provided evidence that metformin treatment can inhibit IL-36γ-mediated IL-23 production in BMDCs, which might contribute to the prevention of psoriasis.


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