title: Accelerated differentiation of bone marrow-derived dendritic cells in atopic prone mice.
abstract: NC/Nga mice are atopic prone mice that can be an animal model for human atopic dermatitis (AD). Dendritic cells (DC) as professional antigen-presenting cells (APC) are the most capable inducers of immune responses. The present study using BALB/c, C57BL/6J, and NC/Nga male mice investigated whether differentiation and function of DC were associated with atopic prone. Bone marrow-derived DC (BMDC) were differentiated by culture with granulocyte macrophage colony stimulating factor (GM-CSF). At days 0, 6, and 8 of culture with GM-CSF, the expression of MHC class II, co-stimulatory molecules (CD80, CD86), and of DC markers (CD11c, DEC205) was measured by flow cytometry. Antigen-presenting activity of BMDC and cytokine production were measured by ELISA. The cell numbers and the expression of MHC class II, co-stimulatory molecules, and of DC markers on BMDC from NC/Nga mice were significantly larger than those from BALB/c and C57BL/6J mice. Antigen-presenting activity of BMDC was significantly greater in NC/Nga and C57BL/6J mice than in BALB/c mice. BMDC-stimulated IFN-gamma production from T-cells was significantly lower in NC/Nga or BALB/c mice than in C57BL/6J mice, whereas IL-4 production was significantly greater in NC/Nga and C57BL/6J mice than in BALB/c mice. Taken together, GM-CSF-stimulated differentiation of BMDC was more accelerated in atopic prone NC/Nga mice than in the other strains of mice. The enhancement of differentiation and function of DC caused by genetic background may be related, at least partly, to the induction or aggravation of allergic/atopic diseases.
authors.affiliation: Environmental Health Sciences Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan. ekoike@nies.go.jp
authors.forename: Eiko
authors.initials: E
authors.lastname: Koike
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
mesh_terms: D000818:Animals; D018122:B7-1 Antigen / Q000276:immunology / Q000378:metabolism; D051940:B7-2 Antigen / Q000276:immunology / Q000378:metabolism; D001854:Bone Marrow Cells / Q000187:drug effects / Q000276:immunology*; D039521:CD11c Antigen / Q000276:immunology / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology*; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D015847:Interleukin-4 / Q000096:biosynthesis / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains
chemical_list: D018122:B7-1 Antigen; D051940:B7-2 Antigen; D039521:CD11c Antigen; D015847:Interleukin-4; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor