作者: Zhi-Hua Cui , Anthony Joetham , M. Kemal Aydintug , Yoon-Soo Hahn , Willi K. Born
DOI: 10.1164/RCCM.200305-634OC
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摘要: Long-term allergen exposure can attenuate inflammation and revert airway hyperreactivity to normal responsiveness. A model of such reversal was established in which ovalbumin-sensitized challenged mice were decreased after multiple daily challenges. This change responsiveness associated with a transition from helper T cell Type 2 1 cytokine-biased profile bronchoalveolar lavage fluid. Cell transfer long-term exposed into hyperreactive also restored responsiveness, establishing the mechanism underlying as active suppression, but did not affect eosinophilic inflammation. Conversely, hyperreactivity, suppressed result exposure, could be reestablished by depleting cells, particular V4 cells. Antigen-specific tolerance cells or suppression non- play role regulation allergic inflammatory response. These findings show that previously mice, achieved challenge, is based on several, apparently independent regulatory mechanisms. One these, focused involves requires