Essential role of CD4+ T cells for the activation of group 2 innate lymphoid cells during respiratory syncytial virus infection in mice

被引:11
|
作者
Han, Xu [1 ,2 ]
Bai, Song [1 ]
Cui, Yulin [1 ]
Zhu, Wenwen [1 ]
Zhao, Na [1 ]
Liu, Beixing [1 ]
机构
[1] China Med Univ, Dept Pathogen Biol, Sch Basic Med Sci, Shenyang, Peoples R China
[2] China Med Univ, Dept Med Oncol, Affiliated Hosp 1, Shenyang, Peoples R China
基金
中国国家自然科学基金;
关键词
activation; CD4(+) T cells; group 2 innate lymphoid cells; IL-2; respiratory syncytial virus; NATURAL HELPER-CELLS; TYPE-2; IMMUNITY; LUNG; CYTOKINES; ASTHMA; IL-2; SENSITIZATION; INFLAMMATION; PATHWAY; PRODUCE;
D O I
10.2217/imt-2019-0084
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Aim: To investigate whether and how CD4(+ )T cells contribute to ILC2 activation during respiratory syncytial virus (RSV) infection. Methods: The methods of flow cytometry, quantitative PCR and ELISA were used in the present study. Results: Depletion of CD4(+) T cells diminished the numbers of lung ILC2s as well as their ability to produce type 2 cytokines. CD4(+ )T cell-mediated ILC2 activation is related to IL-2. The main cellular source of IL-2 was CD4(+ )T cells. Depletion of CD4(+) T cells decreased IL-2 levels in the lungs of RSV-infected mice. IL-2 can directly stimulate ILC2 proliferation and promote ILC2s to produce cytokines. Treatment of mice with neutralizing anti-IL-2 monoclonal antibodies diminished ILC2 activation. Conclusion: These results suggest that CD4(+) T cells contribute to RSV-induced ILC2 activation partly via producing IL-2.
引用
收藏
页码:1303 / 1313
页数:11
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