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Regulatory Role of Lymphoid Chemokine CCL19 and CCL21 in the Control of Allergic Rhinitis¹

Kaoru Takamura^*,, Satoshi Fukuyama^*, Takahiro Nagatake^*, Dong-Young Kim^*,, Aya Kawamura^*, Hideyuki Kawauchi and Hiroshi Kiyono^2,*

^* Division of Mucosal Immunology, Department of Microbiology and Immunology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan; Department of Otorhinolaryngology, The Shimane University School of Medicine, Izumo, Japan; and Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, Korea

The lymphoid chemokines CCL19 and CCL21 are known to be crucial both for lymphoid cell trafficking and for the structural organization of lymphoid tissues such as nasopharynx-associated lymphoid tissue (NALT). However, their role in allergic responses remains unclear, and so our current study aims to shed light on the role of CCL19/CCL21 in the development of allergic rhinitis. After nasal challenge with OVA, OVA-sensitized plt (paucity of lymph node T cells) mice, which are deficient in CCL19/CCL21, showed more severe allergic symptoms than did identically treated wild-type mice. OVA-specific IgE production, eosinophil infiltration, and Th2 responses were enhanced in the upper airway of plt mice. Moreover, in plt mice, the number of CD4⁺CD25⁺ regulatory T cells declined in the secondary lymphoid tissues, whereas the number of Th2-inducer-type CD8^–CD11b⁺ myeloid dendritic cells (m-DCs) increased in cervical lymph nodes and NALT. Nasal administration of the plasmid-encoding DNA of CCL19 resulted in the reduction of m-DCs in the secondary lymphoid tissues and the suppression of allergic responses in plt mice. These results suggest that CCL19/CCL21 act as regulatory chemokines for the control of airway allergic disease and so may offer a new strategy for the control of allergic disease.

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 the Core Research for Evolutional Science and Technology (CREST) Program, the Japan Science and Technology Corporation, a Grant-in-Aid from the Ministry of Education, Science, Sports and Culture, and the Ministry of Health. S.F. and T.N. were supported by research fellowships from the Japan Society for the Promotion of Science for Young Scientists. D.-Y.K. was supported by research fellowships from the Japan Society for the Promotion of Science for Foreign Researchers.

² Address correspondence and reprint requests to Dr. Hiroshi Kiyono, Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan. E-mail address: kiyono{at}ims.u-tokyo.ac.jp

³ Abbreviations used in this paper: DC, dendritic cell; plt, paucity of lymph node T cells; NALT, nasopharynx-associated lymphoid tissue; CLN, cervical lymph nodes; Treg, regulatory T cell; AR, allergic rhinitis; m-DC, myeloid DC; NP, nasal passage; l-DC, lymphoid DC; WT, wild type.