The molecular mechanism of ST2-ILC2 secretion il-17 and its inflammatory effect in the inflammatory response of the lungs.

On April 3, Qiu Ju Research Group of the Shanghai Institute of Nutrition and Health of the Chinese Academy of Sciences, in collaboration with Shen Lei Research Group of shanghai Jiaotong University School of Medicine and Sheng Huiming Ofsin Huiming Group of The Inspection Department of Tongren Hospital affiliated with Shanghai Jiaotong University, published an online research paper entitled IL-17-Producing-ST2-ILC2 Plays aooino.
Type 2 natural lymphocytes (Group 2 Innate Lymphoid Cell, ILC2) are a subgroup of inherent immune cells that secrete IL-5 and IL-13 and are reported to play an important role in allergic diseases.
IL-25 and IL-33 can act on ILC2 to amplify and promote its function.
previous studies have found that IL-25 and IL-33 can act on two ILC2s, iILC2 (iiLC2, ST2-IL-17RBhigh and respond to IL-25 signals) and nILC2 (natural ILC2, ST2-IL-17RBlow and response to IL-33 signals).
unlike nILC2, iILC2 expresses IL-17 and plays an immune defense role in lung infections.
and ST2-nILC2 did not have the secretion of IL-17 under steady-state non-infectious conditions.
the study, it was found that ST2-ILC2 secretion of IL-17 can be stimulated under conditions of inflammation of the lungs induced by IL-33 and papaproteinase (papain).
the phenomenon does not depend on adaptive immune systems, i.e. it also exists in Rag1-/-mice where T and B cells lack.
interesting, ST2-ILC2 secretiating IL-17 relies on transcription factor Ahr (aryl hydrocarbon rounder) rather than the classic transcription factor ROR-t, which regulates the expression of multiple immune cells IL-17.
using bone marrow transplanttechnolog, the researchers found that the IL-33 downstream Myd88 signal from the hematopoietic system is essential for ST2-ILC2 secretion IL-17.
However, IL-33 does not directly promote the expression of IL-17 mRNA in ST2-ILC2, but in collaboration with the NFAT signaling pathway mediated by leukotriene.
IL-17-ST2-ILC2 are il-5, IL-13, IL-17-positive cells, such cells than IL-17 deficiency ILC2 in the pulmonary allergic inflammation of the stronger pathogenicity, as shown in the alveoli in the neutrophils and eosic cells increased and stronger tracheostomy sensitivity response.
also found that the persistent expression of IL-17 in ST2 plus ILC2 in the body depended on IL-33, and that the ability of ST2-ILC2 to secrete IL-17 was significantly reduced after the cessation of IL-33 injection;
ILC2 under il-33 effect, which reduces the dynamic changes of IL-17 and GM-CSF, may play an important role in the progression of inflammation of pulmonary allergic diseases.
the study was conducted by PhD students Cai Wei and Qiu Jinxin under the guidance of researchers Qiu Ju, Shen Lei and Sheng Huiming.
the study was helped by He Rui, a professor at Fudan University School of Medicine, Qian Youdian, a researcher at the Shanghai Institute of Nutrition and Health, Guo Xiaohuan, a professor at Tsinghua University, and Zhou Liang, a professor at the University of Florida.
has also received co-financing from the Ministry of Science and Technology, the National Natural Science Foundation of China and the Chinese Academy of Sciences, as well as the shanghai Institute of Nutrition and Health public technology platform and animal platform support.
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