scholarly journals Effect of γ-secretase inhibitor on Th17 cell differentiation and function of mouse psoriasis-like skin inflammation

2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Lei Ma ◽  
Haibo Xue ◽  
Ruiqun Qi ◽  
Yanqin Wang ◽  
Libing Yuan
2013 ◽  
Vol 191 (11) ◽  
pp. 5777-5777 ◽  
Author(s):  
Soufiane Ghannam ◽  
Jérôme Pène ◽  
Gabriel Moquet-Torcy ◽  
Christian Jorgensen ◽  
Hans Yssel

2015 ◽  
Vol 43 (07) ◽  
pp. 1401-1417 ◽  
Author(s):  
Ming-Han Li ◽  
Hsin-Chieh Wu ◽  
Hsin-Jan Yao ◽  
Chi-Chen Lin ◽  
Shu-Fang Wen ◽  
...  

Antrodia cinnamomea (A. cinnamomea) is a Chinese medicinal herb that possesses a broad range of bioactivities, including anti-inflammation. Given that the proinflammatory cytokine IL-17 plays a critical role in the pathogenesis of autoimmune diseases, we investigated whether A. cinnamomea could inhibit the development of Th17 cells, the main producer of IL-17, and exhibit therapeutic effects on an animal model of psoriasis. We found that A. cinnamomea extract (AC) inhibited the differentiation of Th17 cells as well as the production of IL-17A, IL-21, and IL-22 from these cells. This effect was associated with the inhibition of STAT3 phosphorylation and ROR[Formula: see text]t expression. Notably, the oral administration of AC reduced psoriasis-like inflammation in imiquimod-mediated dermal damage, repressed the expression of IL-17A, IL-22, and TNF-[Formula: see text] in skin lesions, and decreased the infiltration of CD4[Formula: see text] T cells, CD8[Formula: see text] T cells, and neutrophils into the dermis. Finally, serum levels of IL-17A were decreased in AC-treated mice with psoriasis-like skin inflammation. Taken together, these findings indicate that AC inhibits Th17 cell differentiation, suggesting a role for A. cinnamomea in the treatment of psoriasis and other Th17 cell-mediated inflammatory diseases.


2010 ◽  
Vol 185 (1) ◽  
pp. 302-312 ◽  
Author(s):  
Soufiane Ghannam ◽  
Jérôme Pène ◽  
Gabriel Torcy-Moquet ◽  
Christian Jorgensen ◽  
Hans Yssel

2021 ◽  
Vol 12 ◽  
Author(s):  
Junxia Huang ◽  
Xinzhi Xu ◽  
Ji Yang

T helper 17 (Th17) cells are characterized by the secretion of the IL-17 cytokine and are essential for the immune response against bacterial and fungal infections. Despite the beneficial roles of Th17 cells, unrestrained IL-17 production can contribute to immunopathology and inflammatory autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. Although these diverse outcomes are directed by the activation of Th17 cells, the regulation of Th17 cells is incompletely understood. The discovery that microRNAs (miRNAs) are involved in the regulation of Th17 cell differentiation and function has greatly improved our understanding of Th17 cells in immune response and disease. Here, we provide an overview of the biogenesis and function of miRNA and summarize the role of miRNAs in Th17 cell differentiation and function. Finally, we focus on recent advances in miRNA-mediated dysregulation of Th17 cell fate in autoimmune diseases.


2009 ◽  
Vol 184 (6) ◽  
pp. i16-i16
Author(s):  
Katia Boniface ◽  
Kristian S. Bak-Jensen ◽  
Ying Li ◽  
Wendy M. Blumenschein ◽  
Mandy J. McGeachy ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Weixi Zhang ◽  
Xueya Zhang ◽  
Anqun Sheng ◽  
Cuiye Weng ◽  
Tingting Zhu ◽  
...  

T helper 17 (Th17) cells play an important role in the pathogenesis of allergic asthma. Th17 cell differentiation requires Notch signaling.γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evaluate the effect of GSI on Th17 cell differentiation in a mouse model of allergic asthma. OVA was used to induce mouse asthma model in the presence and absence of GSI. GSI ameliorated the development of OVA-induced asthma, including suppressing airway inflammation responses and reducing the severity of clinical signs. GSI also significantly suppressed Th17-cell responses in spleen and reduced IL-17 levels in serum. These findings suggest that GSI directly regulates Th17 responses through a Notch signaling-dependent pathway in mouse model of allergic asthma, supporting the notion that GSI is a potential therapeutic agent for the treatment of allergic asthma.


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