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This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: jimmunol.0901349v1 183/3/1523    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Niu, N. Articles by Cohn, L. PubMed PubMed Citation Articles by Niu, N. Articles by Cohn, L. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Substance via MeSH Medline Plus Health Information Allergy

Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation¹

Naiqian Niu^*, Terri Laufer, Robert J. Homer and Lauren Cohn^2,*

^* Section of Pulmonary and Critical Care Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT 06520; and Division of Rheumatology, University of Pennsylvania School of Medicine and Department of Medicine, Philadelphia Veterans Affairs Medical Center, Philadelphia, PA 19104

In allergic airway inflammation, dendritic cells (DCs) are required for Th2 generation, recruitment, and activation in the respiratory tract. DCs have been shown to be necessary and sufficient for the induction of Th1 immune responses. In Th2 immunity and allergic airway inflammation, the ability of a DC to function as the sole APC has not been tested. We show that CD11c/A_β^b mice with MHC class II expression restricted to CD11c-expressing DCs develop airway neutrophilia rather than allergic airway inflammation. Although CD11c/A_β^b mice are capable of Th2 recruitment and activation in the lung, Th2 priming in CD11c/A_β^b mice results in IFN- production. Effective Th2 generation and allergic airway inflammation was achieved in CD11c/A_β^b mice after treatment with anti-IFN-. These studies show that DCs alone cannot drive the development of Th2 cells but require an additional MHC class II signal to stimulate effective Th2 immunity.

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 Institutes of Health Grant R01–64040 (to L.C.) and the Seltzer Family Translational Research Fund (to L.C.).

² Address correspondence and reprint requests to Dr. Lauren Cohn, Yale University School of Medicine, 333 Cedar Street, PO Box 208057, New Haven, CT 06520-8057. E-mail address: lauren.cohn{at}yale.edu

³ Abbreviations used in this paper: MHC II, MHC class II; BAL, bronchoalveolar lavage; DC, dendritic cell; cDC, conventional DC; LN, lymph node; Tg, transgenic.

⁴ The online version of this article contains supplemental material.