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Vγ4+ γδ T Cells Regulate Airway Hyperreactivity to Methacholine in Ovalbumin-Sensitized and Challenged Mice

Authors
 Youn-Soo Hahn  ;  Christian Taube  ;  Willi K. Born  ;  Erwin W. Gelfand  ;  Rebecca L. O’Brien  ;  Michael Lahn  ;  Christina L. Roark  ;  M. Kemal Aydintug  ;  J. M. Wands  ;  Jung-Won Park  ;  Katsuyuki Takeda  ;  Niyun Jin 
Citation
 JOURNAL OF IMMUNOLOGY, Vol.171(6) : 3170-3178, 2003 
Journal Title
 JOURNAL OF IMMUNOLOGY 
ISSN
 0022-1767 
Issue Date
2003
Abstract
The Vγ4+ pulmonary subset of γδ T cells regulates innate airway responsiveness in the absence of αβ T cells. We now have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged mice that exhibit Th2 responses, pulmonary inflammation, and airway hyperreactivity (AHR). In sensitized mice, Vγ4+ cells preferentially increased in number following airway challenge. Depletion of Vγ4+ cells before the challenge substantially increased AHR in these mice, but had no effect on airway responsiveness in normal, nonchallenged mice. Depletion of Vγ1+ cells had no effect on AHR, and depletion of all TCR-δ+ cells was no more effective than depletion of Vγ4+ cells alone. Adoptively transferred pulmonary lymphocytes containing Vγ4+ cells inhibited AHR, but lost this ability when Vγ4+ cells were depleted, indicating that these cells actively suppress AHR. Eosinophilic infiltration of the lung and airways, or goblet cell hyperplasia, was not affected by depletion of Vγ4+ cells, although cytokine-producing αβ T cells in the lung increased. These findings establish Vγ4+ γδ T cells as negative regulators of AHR and show that their regulatory effect bypasses much of the allergic inflammatory response coincident with AHR.
Files in This Item:
T200302919.pdf Download
DOI
10.4049/​jimmunol.171.6.3170
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Park, Jung Won(박중원) ORCID logo https://orcid.org/0000-0003-0249-8749
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/113396
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