Pulmonary T cells and eosinophils: Coconspirators or independent triggers of allergic respiratory pathology?

被引:106
作者
Lee, NA
Gelfand, EW
Lee, JJ
机构
[1] Mayo Clin Scottsdale, Div Hematol Oncol Pulm, Scottsdale, AZ 85259 USA
[2] Mayo Clin Scottsdale, Dept Biochem & Mol Biol, Div Pulm, Scottsdale, AZ 85259 USA
[3] Natl Jewish Med & Res Ctr, Dept Pediat, Div Cell Biol, Denver, CO USA
关键词
T cell; eosinophil; asthma; mouse models; gene knock-out; T-H(2);
D O I
10.1067/mai.2001.116002
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Etiologic discussions of allergic respiratory pathology frequently engender rabid constituencies of pro-T cell or proeosinophil disciples, each claiming, often with religious fervor, the importance of their leukocyte, However increasing evidence suggests that the exclusionary rhetoric from either camp is inadequate to explain many of the pathologic changes occurring in the lung, Data from both asthmatic patient and mouse models of allergic respiratory inflammation suggest that, in addition to cell-autonomous activities, T-cell and eosinophil interactions may be critical to the onset and progression of pulmonary pathology. These studies also suggest that T-lymphocyte subpopulations and eosinophils communicate by means of both direct cell-cell interactions and through the secretion of inflammatory signals. Collectively, the data support an expanded view of T-cell and eosinophil activities in the lung, including both immunoregulative activities and downstream effector functions impinging directly on lung function.
引用
收藏
页码:945 / 957
页数:13
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