Metcalfe Dean D
Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1881, USA.
Blood. 2008 Aug 15;112(4):946-56. doi: 10.1182/blood-2007-11-078097.
Mast cells have been recognized for well over 100 years. With time, human mast cells have been documented to originate from CD34+ cells, and have been implicated in host responses in both innate and acquired immunity. In clinical immunology, they are recognized for their central role in IgE-mediated degranulation and allergic inflammation by virtue of their expression of the high-affinity receptor for IgE and release of potent proinflammatory mediators. In hematology, the clinical disease of mastocytosis is characterized by a pathologic increase of mast cells in tissues, often associated with mutations in KIT, the receptor for stem cell factor. More recently, and with increased understanding of how human mast cells are activated through receptors including the high-affinity receptor for IgE and KIT, specific tyrosine kinase inhibitors have been identified with the potential to interrupt signaling pathways and thus limit the proliferation of mast cells as well as their activation through immunoglobulin receptors.
肥大细胞已被认识超过100年。随着时间的推移,已证明人类肥大细胞起源于CD34+细胞,并参与先天性和获得性免疫中的宿主反应。在临床免疫学中,由于它们表达IgE高亲和力受体并释放强效促炎介质,肥大细胞在IgE介导的脱颗粒和过敏性炎症中发挥核心作用而被人们所认识。在血液学中,肥大细胞增多症的临床疾病特征是组织中肥大细胞病理性增加,常与干细胞因子受体KIT的突变有关。最近,随着对人类肥大细胞如何通过包括IgE高亲和力受体和KIT在内的受体被激活的了解增加,已鉴定出特定的酪氨酸激酶抑制剂,它们有可能中断信号通路,从而限制肥大细胞的增殖及其通过免疫球蛋白受体的激活。