Polymorphonuclear myeloid‐derived suppressor cells attenuate allergic airway inflammation by negatively regulating group 2 innate lymphoid cells. Issue 4 (17th January 2019)

• Record Type: Journal Article
• Authors: Cao, Yingjiao; He, Yumei; Wang, Xiangyang; Liu, Yongdong; Shi, Kun; Zheng, Zheng; Su, Xue; Lei, Aihua; He, Juan; Zhou, Jie
• Is Part Of: Immunology. Volume 156:Issue 4(2019)
• Page Start: 402
• Page End: 412
• Publication Date: 2019-01-17
• Subjects: allergic airway inflammation -- group 2 innate lymphoid cells -- polymorphonuclear myeloid‐derived suppressor cells; Immunology -- Periodicals
• DOI: 10.1111/imm.13040
• Languages: English
• ISSNs: 0019-2805

Abstract

Summary: Hyperactivation of the type 2 immune response is the major mechanism of allergic asthma, in which both group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells participate. Myeloid‐derived suppressor cells (MDSCs) alleviate asthma by suppressing Th2 cells. However, the potential effects of MDSCs on the biological functions of ILC2s remain largely unknown. Here, we examined the roles of MDSCs (MDSCs) in the modulation of ILC2 function. Our results showed that polymorphonuclear (PMN)‐MDSCs, but not monocytic (M‐) MDSCs, effectively suppressed the cytokine production of ILC2s both in vitro and in vivo, thereby alleviating airway inflammation. Further analyses showed that cyclo‐oxygenase‐1 may mediate the suppressive effects of PMN‐MDSCs on ILC2 responses. Our findings demonstrated that PMN‐MDSCs may serve as a potent therapeutic target for the treatment of ILC2‐driven allergic asthma. Abstract : Polymorphonuclear MDSCs could relieve ILC2‐mediated allergic asthma via suppression of ILC2 function, in which cyclooxygenase‐1 may participate.