Journal
CANADIAN RESPIRATORY JOURNAL
Volume 2021, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2021/9999122
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Funding
- Youth Program of National Natural Science Foundation of China [82000032]
- National Natural Science Foundation of China [81470268, 81800087, 81560007, 81760009]
- Natural Science Foundation of Hunan Province [2019JJ50850]
- Science and Technology Base and Talent Special Project of Guangxi Province [AD19110160]
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This study confirms that IL-1 beta, IL-6, anti-IFN-gamma, and IL-21 promote the differentiation of dual-positive Th2-Th17 cells, and a higher proportion of these cells can be obtained through conditioned differentiation of mouse CD4(+) T cells after classical allergic asthma modeling. Prior to asthma modeling, adoptive dual-positive Th2-Th17 cells promoted differentiation of T cells into the same biphenotype cells, exacerbating asthma severity.
Asthma is a heterogeneous disease, and abnormal activation of T cells is the driving link of asthma's pathophysiological changes. Dual-positive Th2-Th17 cells, as newly discovered T-helper cells, have the functions of Th2 and Th17 cells and can coproduce Th2 and Th17 cytokines. Previous studies have shown that dual-positive Th2-Th17 cells increase the chances of asthma and correlate with asthma severity. However, the exact role of dual-positive Th2-Th17 cells in asthma is not known. Since there is no mature differentiation method for dual-positive Th2-Th17 cells, the present study aimed to clarify the strict differentiation conditions and reveal how dual-positive Th2-Th17 cells regulate asthma phenotypes. In this study, we confirmed that IL-1 beta, IL-6, anti-IFN-gamma, and IL-21 promoted biphenotypic cell differentiation. Moreover, more proportion of dual-positive Th2-Th17 cells can be obtained by conditioned differentiation of mouse CD4(+) T cells after classical allergic asthma modeling. Before asthma modeling, adoptive dual-positive Th2-Th17 cells promoted T cells to differentiate into the same biphenotype cells and exacerbated the severity of asthma. Together, our results clarify the differentiation conditions of dual-positive Th2-Th17 cells and further confirm that it stimulates asthma T cells to differentiate into the same biphenotype cells, leading to exacerbation of asthma.
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