Nilsson G, Metcalfe D D
Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Allergy Asthma Proc. 1996 Mar-Apr;17(2):59-63. doi: 10.2500/108854196778645074.
Mast cells are the principal initial effector cells in the modulation of allergic inflammation. They are now known to arise from CD34+ pluripotential stem cells, circulate through the blood as CD34+, Fc epsilon RI-, Kit+ committed but undifferentiated cells, and migrate into tissues where they mature in the presence of Kit-ligand (stem cell factor) and other locally produced cytokines. Mast cells undergo programmed cell death (apoptosis) when stem cell factor is not available. Mast cells adhere to specific connective tissue components such as fibronectin and laminin. This interaction localizes mast cells to specific sites while altering their biologic responsiveness. Mast cells, when activated through Fc epsilon RI, release and generate a wide variety of cytokines including IL-4 and IL-5. This information provides new insights on how allergic reactions may be modified by developing strategies to effect mast cell viability, survival and localization; and the production of inflammatory mediators.
肥大细胞是调节过敏性炎症的主要初始效应细胞。现在已知它们起源于CD34 +多能干细胞，作为CD34 +、FcεRI -、Kit +定向但未分化的细胞在血液中循环，并迁移到组织中，在那里它们在Kit配体（干细胞因子）和其他局部产生的细胞因子存在的情况下成熟。当没有干细胞因子时，肥大细胞会经历程序性细胞死亡（凋亡）。肥大细胞粘附于特定的结缔组织成分，如纤连蛋白和层粘连蛋白。这种相互作用将肥大细胞定位到特定部位，同时改变它们的生物学反应性。肥大细胞通过FcεRI激活后，会释放并产生多种细胞因子，包括IL - 4和IL - 5。这些信息为如何通过制定影响肥大细胞活力、存活和定位以及炎症介质产生的策略来改变过敏反应提供了新的见解。
