The role of human mast cell-derived cytokines in eosinophil biology
The role of human mast cell-derived cytokines in eosinophil biology
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DOI：
10.1089/107999004323065057
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发表时间：
2004-05-01
影响因子：
2.3
通讯作者：
Krishnaswamy, G
中科院分区：
文献类型：
--
作者：
Shakoory, B;Fitzgerald, SM;Krishnaswamy, G
嗜酸性粒细胞介导的疾病，如过敏性哮喘、嗜酸性筋膜炎和某些过敏性肺部疾病，以嗜酸性粒细胞浸润和组织损伤为特征。肥大细胞和T细胞通常共定位于这些区域。最近的数据表明，肥大细胞可以促进嗜酸性粒细胞介导的炎症反应。抗原和免疫球蛋白E（IgE）可通过IgE的高亲和力受体（Fc ε RI）激活肥大细胞。蛋白酶、白三烯、脂质介质和组胺的释放可促进组织炎症并允许嗜酸性粒细胞向组织募集。此外，大量细胞因子和趋化因子的合成和表达（如粒细胞-巨噬细胞集落刺激因子[GM-CSF]、白细胞介素-1 [IL-1]、IL-3、IL-5、肿瘤坏死因子-α [TNF-α]和趋化因子IL-8，其在活化后调节正常T细胞表达和分泌[RANTES]，单核细胞趋化蛋白-1 [MCP-1]，和嗜酸性粒细胞趋化因子）可影响嗜酸性粒细胞生物学。干细胞因子（SCF）-c-kit、丝氨酸-细胞因子受体和趋化因子-趋化因子受体（CCR 3）相互作用导致核因子-κ B（NF-κ B）、促分裂原活化蛋白激酶（MAPK）表达和其他信号传导途径可调节嗜酸性粒细胞功能。嗜酸性粒细胞的造血、活化、存活和介质的产生都可以由组织中的肥大细胞调节。此外，由于嗜酸性粒细胞可以分泌SCF，嗜酸性粒细胞可以调节肥大细胞的功能，在旁分泌的方式。嗜酸性粒细胞和肥大细胞之间的这种双向相互作用可以为各种人类疾病中的慢性炎症反应铺平道路。本文综述了人肥大细胞和嗜酸性粒细胞之间的关键相互作用。
Eosinophil-mediated diseases, such as allergic asthma, eosinophilic fasciitis, and certain hypersensitivity pulmonary disorders, are characterized by eosinophil infiltration and tissue injury. Mast cells and T cells often colocalize to these areas. Recent data suggest that mast cells can contribute to eosinophil-mediated inflammatory responses. Activation of mast cells can occur by antigen and immunoglobulin E (IgE) via the high-affinity receptor (FcepsilonRI) for IgE. The liberation of proteases, leukotrienes, lipid mediators, and histamine can contribute to tissue inflammation and allow recruitment of eosinophils to tissue. In addition, the synthesis and expression of a plethora of cytokines and chemokines (such as granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin-1 [IL-1], IL-3, IL-5, tumor necrosis factor-alpha [TNF-alpha], and the chemokines IL-8, regulated upon activation normal T cell expressed and secreted [RANTES], monocyte chemotactic protein-1 [MCP-1], and eotaxin) by mast cells can influence eosinophil biology. Stem cell factor (SCF)-c-kit, cytokine-cytokine receptor, and chemokine-chemokine receptor (CCR3) interactions leading to nuclear factor-kappaB (NF-kappaB), mitogen-activated protein kinase (MAPK) expression, and other signaling pathways can modulate eosinophil function. Eosinophil hematopoiesis, activation, survival, and elaboration of mediators can all be regulated thus by mast cells in tissue. Moreover, because eosinophils can secrete SCF, eosinophils can regulate mast cell function in a paracrine manner. This two-way interaction between eosinophils and mast cells can pave the way for chronic inflammatory responses in a variety of human diseases. This review summarizes this pivotal interaction between human mast cells and eosinophils.