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Allergic Airway Hyperresponsiveness-Enhancing T Cells Develop in Normal Untreated Mice and Fail to Produce IL-4/13, Unlike Th2 and NKT Cells¹

Niyun Jin^*,, Christina L. Roark^*,, Nobuaki Miyahara, Christian Taube, M. Kemal Aydintug^*,, J. M. Wands^*,, Yafei Huang^*,, Youn-Soo Hahn, Erwin W. Gelfand, Rebecca L. O'Brien^*, and Willi K. Born^2,*,

^* Integrated Department of Immunology, Division of Cell Biology, Department of Pediatrics, National Jewish Health, and University of Colorado, Denver Health Sciences Center, Denver, CO 80206; and Department of Pediatrics, College of Medicine and Medical Research Institute, Chungbuk National University, Cheongju, Korea

Allergic airway hyperresponsiveness (AHR) in OVA-sensitized and challenged mice, mediated by allergen-specific Th2 cells and Th2-like invariant NKT (iNKT) cells, develops under the influence of enhancing and inhibitory T cells. The AHR-enhancing cells belong to the V1⁺ T cell subset, cells that are capable of increasing IL-5 and IL-13 levels in the airways in a manner like Th2 cells. They also synergize with iNKT cells in mediating AHR. However, unlike Th2 cells, the AHR enhancers arise in untreated mice, and we show here that they exhibit their functional bias already as thymocytes, at an HSA^high maturational stage. In further contrast to Th2 cells and also unlike iNKT cells, they could not be stimulated to produce IL-4 and IL-13, consistent with their synergistic dependence on iNKT cells in mediating AHR. Mice deficient in IFN-, TNFRp75, or IL-4 did not produce these AHR-enhancing T cells, but in the absence of IFN-, spontaneous development of these cells was restored by adoptive transfer of IFN--competent dendritic cells from untreated donors. The i.p. injection of OVA/aluminum hydroxide restored development of the AHR enhancers in all of the mutant strains, indicating that the enhancers still can be induced when they fail to develop spontaneously, and that they themselves need not express TNFRp75, IFN-, or IL-4 to exert their function. We conclude that both the development and the cytokine potential of the AHR-enhancing T cells differs critically from that of Th2 cells and NKT cells, despite similar influences of these cell populations on AHR.

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 work was supported by National Institute of Health grants AI40611 and HL65410 to W.K.B., AI44920 and AI063400 to R.L.O., and HL36577 to E.W.G.

² Address correspondence and reprint requests to Dr. Willi K. Born, Integrated Department of Immunology, GB K409, National Jewish Health, 1400 Jackson Street, Denver, CO 80206. E-mail address: bornw{at}njc.org

³ Abbreviations used in this paper: AHR, allergic airway hyperresponsiveness; iNKT, invariant NKT; BAL, bronchoalveolar lavage; DC, dendritic cell; HSA, heat-stable Ag.

This article has been cited by other articles:

				Y. Huang, N. Jin, C. L. Roark, M. K. Aydintug, J. M. Wands, H. Huang, R. L. O'Brien, and W. K. Born The Influence of IgE-Enhancing and IgE-Suppressive {gamma}{delta} T Cells Changes with Exposure to Inhaled Ovalbumin J. Immunol., July 15, 2009; 183(2): 849 - 855. [Abstract] [Full Text] [PDF]