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    Factors affecting the migration of ILC2s in allergic disease. Cellular & molecular immunology 10.1038/s41423-021-00703-x
    Group 2 innate lymphoid cells can engulf and destroy bacteria. Yang Yiran,Li Yan,Xu Yingjie,Zhang Hanxiao,Diao Yuhan,Chen Shihao,Cui Ye,Corrigan Chris J,Wang Wei,Ying Sun Cellular & molecular immunology 10.1038/s41423-021-00765-x
    Repeated exposure to inactivated Streptococcus pneumoniae induces asthma-like pathological changes in mice in the presence of IL-33. Li Chenduo,Du Xiaonan,Huang Qiong,Yang Yiran,Wang Jingjing,Qin Xiaofeng,Wang Wenjun,Liu Zihan,Yuan Huihui,Liu Jie,Lv Zhe,Li Yan,Chen Yan,Cui Ye,Corrigan Chris J,Huang Kewu,Wang Wei,Ying Sun Cellular immunology While environmental aeroallergens and epithelial alarmins such as IL-33 are firmly implicated in asthma, the possible role of Streptococcus pneumoniae (S. pneumoniae) antigens is less clear. To explore this, wild-type BALB/c mice were repeatedly challenged per-nasally with IL-33 and inactivated S. pneumoniae, either agent alone or diluent control. Some animals were rested then later re-challenged with inactivated S. pneumoniae alone. Serum concentrations of S. pneumoniae lysates-specific IgE were measured in patients with asthma and control subjects. Interestingly, in the presence of IL-33, repeated exposure to inactivated S. pneumoniae induced asthma-like pathological changes accompanied by a systemic adaptive immune response. Subsequent re-exposure of the sensitized animals to inactivated S. pneumoniae alone was able to induce such changes. The concentration of S. pneumoniae lysates-specific IgE was significantly elevated in the asthma patients. These data suggest that antigens derived from infectious microorganisms may participate in generating the mucosal inflammation which characterizes asthma. 10.1016/j.cellimm.2021.104438