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Published ahead of print on September 11, 2003, doi:10.1164/rccm.200305-634OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 1324-1332, (2003)
© 2003 American Thoracic Society

Reversal of Allergic Airway Hyperreactivity after Long-term Allergen Challenge Depends on {gamma}{delta} T Cells

Zhi-Hua Cui, Anthony Joetham, M. Kemal Aydintug, Yoon-Soo Hahn, Willi K. Born and Erwin W. Gelfand

Program in Cell Biology, Department of Pediatrics, and Department of Immunology, National Jewish Medical and Research Center, Denver, Colorado

Correspondence and requests for reprints should be addressed to Erwin W. Gelfand, M.D., National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206. E-mail: gelfande{at}njc.org

Long-term allergen exposure can attenuate inflammation and revert airway hyperreactivity to normal responsiveness. A model of such reversal was established in which airway hyperreactivity and inflammation in ovalbumin-sensitized and challenged mice were decreased after multiple daily airway challenges. This change in responsiveness and inflammation was associated with a transition from a helper T cell Type 2 to a helper T cell Type 1 cytokine-biased profile in bronchoalveolar lavage fluid. Cell transfer from long-term exposed mice into hyperreactive mice also restored normal airway responsiveness, establishing the mechanism underlying the reversal of the hyperreactivity as active suppression, but did not affect eosinophilic airway inflammation. Conversely, airway hyperreactivity, suppressed as a result of long-term allergen exposure, could be reestablished by depleting {gamma}{delta} T cells, in particular V{gamma}4+ cells. Antigen-specific tolerance of {alpha}ß T cells or suppression by non-{gamma}{delta} T cells did not play a role in the reversal to normal airway responsiveness and {gamma}{delta} T cells did not play a role in the regulation of the allergic inflammatory response. These findings show that normal responsiveness in previously hyperreactive mice, achieved after long-term allergen challenge, is based on several, apparently independent regulatory mechanisms. One of these, focused on airway responsiveness, involves active suppression and requires {gamma}{delta} T cells.

Key Words: cellular activation • cytokines • mast cells/basophils • signal transduction




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