Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 107, Issue 6, Pages 945-957Publisher
MOSBY-ELSEVIER
DOI: 10.1067/mai.2001.116002
Keywords
T cell; eosinophil; asthma; mouse models; gene knock-out; T-H(2)
Categories
Funding
- NHLBI NIH HHS [HL-61005, HL-60793, HL-58723, HL-65228, HL-36577] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available