title: Role of F4/80+ cells during induction of hapten-specific contact hypersensitivity.
abstract: F4/80, a monoclonal antibody that binds to a surface molecule on mature macrophages and certain dendritic cells, has been used to explore the role of epidermal and dermal cells as antigen-presenting cells (APC) during the induction of contact hypersensitivity (CH) in mice. Systemic administration of the antibody appeared to have little or no physical or functional effect on intraepidermal Langerhans' cells, even though a subpopulation of these cells expressed the F4/80 ligand. None the less, systematically administered F4/80 antibodies were able to impair CH induction when dinitrofluorobenzene (DNFB) was painted on normal body wall skin of BALB/c mice [an ultraviolet B (UVB)-resistant strain]. Interestingly, systemic F4/80 antibodies did not affect CH induction in C57BL/10 mice (a UVB-susceptible strain). When a sensitizing dose of hapten was injected intracutaneously (i.c.) into F4/80-treated BALB/c and C57BL/10 mice, CH induction was impaired in both inbred strains, although the severity of impairment was greater in BALB/c mice. Following UVB radiation of body wall skin, anti-F4/80-treated BALB/c mice displayed very feeble CH, whether hapten was painted epicutaneously or injected i.c. at the irradiated site. Based on these and other recent reported results, it is concluded that (1) BALB/c mice rely partially upon dermal, F4/80+ cells as a source of APC when hapten is applied epicutaneously, whereas C57BL/10 mice rely almost exclusively upon epidermal Langerhans' cells in this circumstance; and (2) after UVB radiation of skin, BALB/c mice can use F4/80+ dermal cells as the source of APC function when hapten is painted epicutaneously. These findings are discussed with respect to the cellular basis for the differential susceptibilities of genetically defined strains of mice to the deleterious effects of UVB radiation on CH induction.
authors.affiliation: Schepens Eye Research Institute, Department of Dermatology, Harvard Medical School, Boston, MA, USA.
authors.forename: I
authors.initials: I
authors.lastname: Kurimoto
authors.forename: S F
authors.initials: SF
authors.lastname: Grammer
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: J W
authors.initials: JW
authors.lastname: Streilein
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000528:radiation effects; D000938:Antigen-Presenting Cells / Q000276:immunology*; D000943:Antigens, Differentiation / Q000032:analysis*; D003877:Dermatitis, Contact / Q000276:immunology*; D004817:Epidermis / Q000276:immunology; D006241:Haptens / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007801:Langerhans Cells / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D012867:Skin / Q000276:immunology*; D014466:Ultraviolet Rays
chemical_list: D000943:Antigens, Differentiation; D006241:Haptens; D000949:Histocompatibility Antigens Class II; C036763:monocyte-macrophage differentiation antigen