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T Cells and NKT Cells1









* Integrated Department of Immunology, National Jewish Medical and Research Center, Denver, CO 80206;
University of Colorado at Denver Health Sciences Center, Denver, CO 80206; and
Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206
Mice sensitized and challenged with OVA were used to investigate the role of innate T cells in the development of allergic airway hyperresponsiveness (AHR). AHR, but not eosinophilic airway inflammation, was induced in T cell-deficient mice by small numbers of cotransferred 
T cells and invariant NKT cells, whereas either cell type alone was not effective. Only V
1+V
5+ 
T cells enhanced AHR. Surprisingly, OVA-specific
β T cells were not required, revealing a pathway of AHR development mediated entirely by innate T cells. The data suggest that lymphocytic synergism, which is key to the Ag-specific adaptive immune response, is also intrinsic to T cell-dependent innate responses.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This study was supported by National Institutes of Health Grants HL65410 and AI40611 (to W.K.B.), AI44920 and AI063400 (to R.L.O.), HL36577 and HL61005 (to E.W.G.), and AI057485 (to L.G.), and by Environmental Protection Agency Grant R825702 (to E.W.G.). Support was also provided by a postdoctoral fellowship from the American Cancer Society (to J.L.M.).
2 Address correspondence and reprint requests to Dr. Willi K. Born, Integrated Department of Immunology, National Jewish Medical and Research Center, 1400 Jackson Street, GB K409, Denver, CO 80206. E-mail address: bornw{at}njc.org
3 Abbreviations used in this paper: iNKT, invariant NKT;
GalCer,
-galactosylceramide; AHR, airway hyperresponsiveness; β2m, β2-microglobulin; BAL, bronchoalveolar lavage; Cdyn, dynamic compliance; DC, dendritic cell; MCh, methacholine; NAD, nonadherent; RL, lung resistance.
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