title: Role of CD4(+) CD25(+) regulatory T cells in T helper 2 cell-mediated allergic inflammation in the airways.
abstract: It has recently been shown that CD4(+) CD25(+) T cells are immunoregulatory T cells that prevent CD4(+) T cell-mediated organ-specific autoimmune diseases. To determine whether CD4(+) CD25(+) T cells downregulate Th2 cell-mediated allergic inflammation in the airways, we studied antigen-induced eosinophil recruitment in the airways in BALB/c Rag-2(-)(/-) mice transferred with CD4(+) CD25(+) T cell-depleted or unfractionated T cells from ovalbumin-specific TCR transgenic mice. Antigen-induced eosinophil recruitment into the airways was significantly decreased in the mice transferred with CD4(+) CD25(+) T cell-depleted splenocytes as compared with those transferred with unfractionated splenocytes. On the other hand, the depletion of CD4(+) CD25(+) T cells increased antigen-induced neutrophil and T cell recruitment in the airways of the mice. The depletion of CD4(+) CD25(+) T cells also decreased antigen-induced IL-4 and IL-5 production in the airways of the mice. Finally, the depletion of CD4(+) CD25(+) T cells prevented antigen-induced Th2 cell differentiation in vitro but increased the differentiation of Th1 cells. These results indicate that CD4(+) CD25(+) T cells modulate the Th1 and Th2 cell balance toward Th2 cells and thus upregulate Th2 cell-mediated allergic inflammation in the airways.
authors.affiliation: Department of Internal Medicine II, Chiba University School of Medicine, Chiba, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Suto
authors.forename: H
authors.initials: H
authors.lastname: Nakajima
authors.forename: S I
authors.initials: SI
authors.lastname: Kagami
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: Y
authors.initials: Y
authors.lastname: Saito
authors.forename: I
authors.initials: I
authors.lastname: Iwamoto
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D015704:CD4 Antigens / Q000276:immunology*; D002454:Cell Differentiation; D002478:Cells, Cultured; D016207:Cytokines / Q000032:analysis / Q000276:immunology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000276:immunology*; D004804:Eosinophils / Q000276:immunology*; D006967:Hypersensitivity / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D015847:Interleukin-4 / Q000032:analysis / Q000276:immunology; D015848:Interleukin-5 / Q000032:analysis / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D008822:Mice, Transgenic; D020556:Neutrophil Infiltration; D015375:Receptors, Interleukin-2 / Q000276:immunology*; D013154:Spleen / Q000166:cytology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D015854:Up-Regulation / Q000276:immunology*
chemical_list: D015704:CD4 Antigens; D016207:Cytokines; D015848:Interleukin-5; D015375:Receptors, Interleukin-2; D015847:Interleukin-4