Negative feedback on IL-23 exerted by IL-17A during pulmonary inflammation:

Innate Immunity

ElinSilverpil¹ 

关键词: IL-17;    IL-23;    macrophages;    neutrophils;    airway inflammation;    Rac1;    bronchoalveolar lavage;    host defense;    mouse;    human;   

DOI  :  10.1177/1753425912470470

学科分类：生物科学（综合）

来源: Sage Journals

【 摘 要 】

It is now established that IL-17 has a broad pro-inflammatory potential in mammalian host defense, in inflammatory disease and in autoimmunity, whereas little is known about its anti-inflammatory potential and inhibitory feedback mechanisms. Here, we examined whether IL-17A can inhibit the extracellular release of IL-23 protein, the upstream regulator of IL-17A producing lymphocyte subsets, that is released from macrophages during pulmonary inflammation. We characterized the effect of IL-17A on IL-23 release in several models of pulmonary inflammation, evaluated the presence of IL-17 receptor A (RA) and C (RC) on human alveolar macrophages and assessed the role of the Rho family GTPase Rac1 as a mediator of the effect of IL-17A on the release of IL-23 protein. In a model of sepsis-induced pneumonia, intravenous exposure to Staphylococcus aureus caused higher IL-23 protein concentrations in cell-free bronchoalveolar lavage (BAL) samples from IL-17A knockout (KO) mice, compared with wild type (WT) control m...

【 授权许可】

CC BY