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Institute of Immunology, Hannover Medical School, Hannover, Germany
Allergic airway diseases such as asthma are caused by a failure of the immune system to induce tolerance against environmental Ags. The underlying molecular and cellular mechanisms that initiate tolerance are only partly understood. In this study, we demonstrated that a CCR7-dependent migration of both CD103+ and CD103– lung dendritic cells (DC) to the bronchial lymph node (brLN) is indispensable for this process. Although inhaled Ag is amply present in the brLN of CCR7-deficient mice, T cells cannot be tolerized because of the impaired migration of Ag-carrying DC and subsequent transport of Ag from the lung to the draining lymph node. Consequently, the repeated inhalation of Ag protects wild-type but not CCR7-deficient mice from developing allergic airway diseases. Thus, the continuous DC-mediated transport of inhaled Ag to the brLN is critical for the induction of tolerance to innocuous Ags.
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 has been supported by Deutsche Forschungsgemeinschaft Grant SFB587-B3 (to R.F.).
2 Address correspondence and reprint requests to Prof. Dr. Reinhold Förster, Institute of Immunology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. E-mail address: foerster.reinhold{at}mh-hannover.de
3 Abbreviations used in this paper: DC, dendritic cell; DLN, draining lymph node; brLN, bronchial LN; BM, bone marrow; i.t., intratracheal(ly); LN, lymph node; MHCII, MHC class II; DAPI, 4',6'-diamidino-2-phenylindole; BAL, bronchoalveolar lavage; CD62L, pDC, plasmacytoid.
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