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Angiotensin Ⅱ enhances the group 2 innate lymphoid cells responses via its receptor AT1a during airway inflammation

Angiotensin Ⅱ enhances the group 2 innate lymphoid cells re...

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第十四届全国免疫学学术大会

作者： Gaoyu Liu Yingying Chen Ying Wang Xiaohui Deng Kai Deng Zhi Yao Jie Zhou Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education Department of ImmunologySchool of Basic SciencesTianjin Medical University 中山大学中山医学院中山大学附属第七医院(深圳)

Group 2 innate lymphoid cells(ILC2 s) both contribute to maintain mucosal tissue homeostasis and initiate tissue airway inflammation during allergen challenge,especially during allergic inflammation and worm *** exists crosstalk between the neuro-and epithelial-derived factors and immune cells,which plays an important role in inflammation and tissue homeostasis during allergen challenge.H owever,the detailed and fine mechanism of how epithelium-derived peptides control ILC2 s(this biological process) remains to be fully *** this study,we found that lung epithelial cells express angiotensinogen(AGT) and the components of RAS,including AGT,renin,ACE were upregulated during allergen papain challenge by using immunofluorescence staining(IF) and laser confocal imaging technology and in vivo papain-induced lung inflammation ***2 s expressed relatively higher levels of the Ang II receptor AT1 a,and colocalized with lung epithelial cells expressing *** of Ang II significantly potentiated ILC2 responses both in vivo and in vitro,which were almost completely abrogated in AT1 a-deficient *** transfer of ILC2 into immunodeficient NCG mice and mixed bone marrow chimeras experiment support that the regulation of ILC2 by Ang II was cell *** of RAS signaling by either angiotensin converting enzyme(ACE) inhibitor captopril or AT1 antagonist telmisartan clearly alleviated the severity of airway inflammation in the context of ILC2-mediated allergic *** studies showed that the regulation of ILC2 by Ang II was associated with marked changes in transcriptional profiling by SMART-seq2,and the activation of Ras-ERK and MAPK signaling pathways,and the phosphorylation of ERK1/2 in ILC2 was sig nificantly induced by AngⅡ.Importantly,the decreased of ILC2 s’ activation by telmisartan was similarly observed in humanized mice after IL-33 challenge,resulted in lesser infiltrated cells in the perib

关键词： ILC2s Ang Ⅱ airway allergic inflammation

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