China
Africa
Explore chapters and articles related to this topic
Immunology of Allergic Diseases
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Besides the nuocyte, TH9 cells are implicated in asthma. It remains to be established whether IL-9 secreting T cells are distinct from TH2 cells or whether TH2 cells differentiate into TH9 cells. TH9 cells do not express the well-defined transcription factors such as T-bet (for TH1), GATA-3 (for TH2) RORγ3 for TH17 and Foxp3 (for iTregs). TH9 cells secrete IL9 that not only promotes mucous production but also synergizes with IL-4 and stem cell factor to promote mast cell development. In concert with IL-13 and TGF-β it contributes to airway remodeling (Holgate 2012).
IL-27 overexpression alleviates inflammatory response in allergic asthma by inhibiting Th9 differentiation and regulating Th1/Th2 balance
Published in Immunopharmacology and Immunotoxicology, 2022
Peng Xiong, Tonglin Liu, Hao Huang, Yi Yuan, Wendi Zhang, Lina Fu, Yu Chen
When Th1 is activated, IFN-γ receptor signal activates STAT1 and promotes the expression of Th1 restrictive transcription factors T-bet and IL-12R. IL-12R can further promote the high expression of T-bet through STAT4 and enhance the phenotype of Th1 cells by promoting the expression of IFN-γ and IL-12Rβ2. Studies have shown that Th9 cells play an important role in allergic diseases. The main effector of immune regulation is IL-9. IL-9 secreted by Th9 cells can act on different inflammatory cells, such as lymphocytes, eosinophils, and mast cells, in turn increasing the number of inflammatory cells and secreting inflammatory mediators to promote inflammation [24]. In addition to acting on inflammatory cells, IL-9 also acts on normal cells, such as smooth muscle cells and airway epithelial cells, which secrete pro-inflammatory factors and produce a large number of goblet cells that secrete large amounts of mucus [25]. In this study, IL-27 OV significantly decreased the expression of IL-9, pSTAT3, and pSTAT1 but significantly increased that of T-bet, and lung tissue inflammatory response was decreased. The findings suggested that IL-27 OV inhibited the secretion of IL-9 by Th9 cells, promoted the activation of Th1 cells, and enhanced the phenotype of Th1 cells.
Modified BuShenYiQi formula alleviates experimental allergic asthma in mice by negative regulation of type 2 innate lymphoid cells and CD4+ type 9 helper T cells and the VIP–VPAC2 signalling pathway
Published in Pharmaceutical Biology, 2021
Muhua Huang, Jinfeng Wu, Jingcheng Dong
ILC2s and Th9 cells act as central initiators and amplifiers of type 2 immune responses in asthma (von Moltke and Pepper 2018). They play cooperative roles in many of the pathophysiological abnormalities characterizing asthma (Ying et al. 2016; Koch et al. 2017; Moretti et al. 2017). To further evaluate whether M-BYF has regulatory effects on ILC2s and Th9 cells, the percentages of these cells in the lungs were determined by flow cytometric analysis. ILC2s were defined as CD45+Lineage (Lin)–ST2+CD90.2+CD127+ cells. Th9 cells were defined as CD45+CD4+IL-9+ cells. Gating strategies of lung ILC2s and Th9 cells are shown in Figure 6(A,D). The percentages of lung ILC2s and Th9 cells were significantly increased in the Model group when compared to the Control group (p < 0.001) (Figure 6(B,C,E,F)). Treatment with three different doses of M-BYF (7, 14 and 28 g/kg/d) and 1 mg/kg/d dose of dexamethasone significantly reduced the percentages of ILC2s and Th9 cells in the lungs of asthmatic mice, as compared with untreated asthmatic mice (p < 0.01 or 0.001). There was no significant difference in the percentage of Th9 cells between the high-dose of M-BYF (28 g/kg/d) treated group and dexamethasone treated group (p > 0.05). Moreover, the effect of high-dose of M-BYF on decrease of ILC2s appeared to be stronger than that of dexamethasone (p < 0.001) (Figure 6(B,C,E,F)).
Immunopathogenesis of inflammatory bowel disease and mechanisms of biological therapies
Published in Scandinavian Journal of Gastroenterology, 2018
Bani Ahluwalia, Luiza Moraes, Maria K. Magnusson, Lena Öhman
Increased numbers of a newly identified effector T-cell subset, termed Th9 cells, has been reported in the intestinal mucosa of UC patients [93,94]. Th9 cells, characterized by production of IL-9, are induced by IL-4 and TGF-β in the presence of several transcriptional factors including PU.1 and interferon regulatory factor 4 [94–97]. IL-9 is suggested to impair gut barrier function, by blocking the proliferation of intestinal epithelial cells and down-regulating the expression of several tight-junction proteins including claudin and occludin [95]. Studies using mouse colitis models as well as patients with IBD report increased numbers of lamina propria IL-9 producing Th9 cells, which suggests a crucial role of Th9 cells in promoting chronic intestinal inflammation [95]. In addition, the mucosal levels of IL-9 may also reflect disease activity, as seen by the higher IL-9 levels reported in UC patients with severe disease as compared with patients with mild disease and control patients [93]. Although the role of Th9 cells has been evaluated mainly via experimental colitis models, the increased number of Th9 cells seen in IBD patients during active disease suggests that controlling the abundance and activity of Th9 cells may be a strategy for treatment [93,95,97].