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T Cell Subsets in Regulating Airway Responsiveness: V1+ Cells, but Not V4+ Cells, Promote Airway Hyperreactivity, Th2 Cytokines, and Airway Inflammation1
* Department of Immunology, and
Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206;
Department of Pediatrics, Chungbuk National University and College of Medicine, Heungdeok-Gu, Cheongju, Korea; and
Department of Pathology, University of Vermont, Colchester, VT 05446
Allergic airway inflammation and hyperreactivity are modulated by 
T cells, but different experimental parameters can influence the effects observed. For example, in sensitized C57BL/6 and BALB/c mice, transient depletion of all TCR-+ cells just before airway challenge resulted in airway hyperresponsiveness (AHR), but caused hyporesponsiveness when initiated before i.p. sensitization. V4+ T cells strongly suppressed AHR; their depletion relieved suppression when initiated before challenge, but not before sensitization, and they suppressed AHR when transferred before challenge into sensitized TCR-V4-/-/6-/- mice. In contrast, V1+ T cells enhanced AHR and airway inflammation. In normal mice (C57BL/6 and BALB/c), enhancement of AHR was abrogated only when these cells were depleted before sensitization, but not before challenge, and with regard to airway inflammation, this effect was limited to C57BL/6 mice. However, V1+ T cells enhanced AHR when transferred before challenge into sensitized B6.TCR--/- mice. In this study V1+ cells also increased levels of Th2 cytokines in the airways and, to a lesser extent, lung eosinophil numbers. Thus, V4+ cells suppress AHR, and V1+ cells enhance AHR and airway inflammation under defined experimental conditions. These findings show how T cells can be both inhibitors and enhancers of AHR and airway inflammation, and they provide further support for the hypothesis that TCR expression and function cosegregate in T cells.
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