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Regulatory role of lymphoid chemokine CCL19 and CCL21 in the control of allergic rhinitis

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Authors

Takamura, Kaoru; Fukuyama, Satoshi; Nagatake, Takahiro; Kim, Dong-Young; Kawamura, Aya; Kawauchi, Hideyuki; Kiyono, Hiroshi

Issue Date
2007
Publisher
American Association of Immunologists
Citation
J. Immunol. 179, 5897-5906
Keywords
Cell DifferentiationChemokine CCL19/genetics/*metabolismChemokine CCL21/genetics/*metabolismDNA/geneticsDendritic Cells/cytologyHypersensitivity/metabolism/pathologyImmunoglobulin E/biosynthesis/immunologyLymphocyte CountLymphoid Tissue/*metabolismMice, Inbred BALB CRhinitis/*metabolism/pathologyT-Lymphocytes, Regulatory/cytologyTh1 Cells/metabolismTh2 Cells/metabolism
Abstract
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 CD8alpha(-)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.
ISSN
0022-1767 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17947663

https://hdl.handle.net/10371/11165
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