title: Differential regulatory function of resting and preactivated allergen-specific CD4+ CD25+ regulatory T cells in Th2-type airway inflammation.
abstract: Although CD4(+)CD25(+) regulatory T (Treg) cells are known to suppress Th1 cell-mediated immune responses, their effect on Th2-type immune responses remains unclear. In this study we examined the role of Treg cells in Th2-type airway inflammation in mice. Depletion and reconstitution experiments demonstrated that the Treg cells of naive mice effectively suppressed the initiation and development of Th2-driven airway inflammation. Despite effective suppression of Th2-type airway inflammation in naive mice, adoptively transferred, allergen-specific Treg cells were unable to suppress airway inflammation in allergen-presensitized mice. Preactivated allergen-specific Treg cells, however, could suppress airway inflammation even in allergen-presensitized mice by accumulating in the lung, where they reduced the accumulation and proliferation of Th2 cells. Upon activation, allergen-specific Treg cells up-regulated CCR4, exhibited enhanced chemotactic responses to CCR4 ligands, and suppressed the proliferation of and cytokine production by polarized Th2 cells. Collectively, these results demonstrated that Treg cells are capable of suppressing Th2-driven airway inflammation even in allergen-presensitized mice in a manner dependent on their efficient migration into the inflammatory site and their regulation of Th2 cell activation and proliferation.
authors.affiliation: Department of Cellular and Molecular Immunology, Mie University Graduate School of Medicine, Tsu, Japan.
authors.forename: Kanako
authors.initials: K
authors.lastname: Saito
authors.forename: Mie
authors.initials: M
authors.lastname: Torii
authors.forename: Ning
authors.initials: N
authors.lastname: Ma
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tsuchiya
authors.forename: Linan
authors.initials: L
authors.lastname: Wang
authors.forename: Tomohide
authors.initials: T
authors.lastname: Hori
authors.forename: Daisuke
authors.initials: D
authors.lastname: Nagakubo
authors.forename: Nao
authors.initials: N
authors.lastname: Nitta
authors.forename: Shiro
authors.initials: S
authors.lastname: Kanegasaki
authors.forename: Kunio
authors.initials: K
authors.lastname: Hieshima
authors.forename: Osamu
authors.initials: O
authors.lastname: Yoshie
authors.forename: Esteban C
authors.initials: EC
authors.lastname: Gabazza
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Katayama
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shiku
authors.forename: Kagemasa
authors.initials: K
authors.lastname: Kuribayashi
authors.forename: Takuma
authors.initials: T
authors.lastname: Kato
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D049109:Cell Proliferation; D016207:Cytokines / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D010047:Ovalbumin / Q000276:immunology; D011014:Pneumonia / Q000139:chemically induced / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D010047:Ovalbumin