趋化因子
炎症
免疫学
脱颗粒
免疫系统
组胺
CCL5
肥大细胞
单因子
四氯化碳
细胞因子
生物
细胞生物学
T细胞
药理学
白细胞介素2受体
生物化学
受体
作者
Pio Conti,A. Caraffa,Gianpaolo Ronconi,S. K. Kritas,F Mastrangelo,L Tettamanti,Theoharis C. Theoharides
标识
DOI:10.1016/j.ejphar.2017.09.044
摘要
Mast cells (MCs) are implicated in an array of diseases, especially those involving a mucosal surface, including intestine. On appropriate activation from cytoplasmatic granules, MCs release preformed chemical mediators and generate inflammatory lipids and cytokines/chemokines. Intracellular signal and Lyn activation pathways can cause the degranulation of MCs and the generation of lipid mediators and cytokines/chemokines. MCs undergo maturation and polarization in gut mucosal surfaces where they are constitutively present, and can alter intestinal permeability, an important factor in many inflammatory mucosal disorders including autoimmune diseases. On the other hand, since they are immununosuppressive, MCs have potential anti-inflammatory properties by producing TGF-β1, interleukin (IL)-4, IL-10, IL-13 and histamine. In addition, MC chymase, located in the sub-mucosa, acts on intestinal permeability by protecting the bowel. To carry the inflammatory response, MCs need to be attracted by CC chemokines such as RANTES (CCL5) and MCP-1(CCL2), an effect absent in genetically W/Wv mast cell-deficient mice, where the inflammatory reaction is not present. Here, we focused our attention on recent findings regarding how MCs can initiate and develop the cellular immune response in the gut and mediate inflammation, an effect that can be inhibited by IL-37. These studies contribute to clarify the mechanisms by which MCs profoundly affect immunity and inflammation of the intestine.
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