title: Regulatory role of lymphoid chemokine CCL19 and CCL21 in the control of allergic rhinitis.
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.
authors.affiliation: Division of Mucosal Immunology, Department of Microbiology and Immunology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
authors.forename: Kaoru
authors.initials: K
authors.lastname: Takamura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fukuyama
authors.forename: Takahiro
authors.initials: T
authors.lastname: Nagatake
authors.forename: Dong-Young
authors.initials: DY
authors.lastname: Kim
authors.forename: Aya
authors.initials: A
authors.lastname: Kawamura
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Kawauchi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kiyono
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D054415:Chemokine CCL19 / Q000235:genetics / Q000378:metabolism*; D054421:Chemokine CCL21 / Q000235:genetics / Q000378:metabolism*; D004247:DNA / Q000235:genetics; D003713:Dendritic Cells / Q000166:cytology; D006967:Hypersensitivity / Q000378:metabolism / Q000473:pathology; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000276:immunology; D018655:Lymphocyte Count; D008221:Lymphoid Tissue / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D012220:Rhinitis / Q000378:metabolism* / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000166:cytology; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D054415:Chemokine CCL19; D054421:Chemokine CCL21; D007073:Immunoglobulin E; D004247:DNA