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Polymorphonuclear myeloid‐derived suppressor cells attenuate allergic airway inflammation by negatively regulating group 2 innate lymphoid cells
Author(s) -
Cao Yingjiao,
He Yumei,
Wang Xiangyang,
Liu Yongdong,
Shi Kun,
Zheng Zheng,
Su Xue,
Lei Aihua,
He Juan,
Zhou Jie
Publication year - 2019
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13040
Subject(s) - innate lymphoid cell , immunology , myeloid derived suppressor cell , immune system , allergic inflammation , inflammation , myeloid , suppressor , cytokine , interleukin 13 , innate immune system , biology , cancer research , interleukin 4 , medicine , cancer
Summary Hyperactivation of the type 2 immune response is the major mechanism of allergic asthma, in which both group 2 innate lymphoid cells ( ILC 2s) and type 2 helper T (Th2) cells participate. Myeloid‐derived suppressor cells ( MDSC s) alleviate asthma by suppressing Th2 cells. However, the potential effects of MDSC s on the biological functions of ILC 2s remain largely unknown. Here, we examined the roles of MDSC s ( MDSC s) in the modulation of ILC 2 function. Our results showed that polymorphonuclear ( PMN )‐ MDSC s, but not monocytic (M‐) MDSC s, effectively suppressed the cytokine production of ILC 2s both in vitro and in vivo , thereby alleviating airway inflammation. Further analyses showed that cyclo‐oxygenase‐1 may mediate the suppressive effects of PMN ‐ MDSC s on ILC 2 responses. Our findings demonstrated that PMN ‐ MDSC s may serve as a potent therapeutic target for the treatment of ILC 2‐driven allergic asthma.