title: Antigen-presenting cells in human periodontal disease tissues.
abstract: T cells are present in the inflammatory infiltrates of periodontal disease lesions and require antigen presentation by antigen-presenting cells (APCs). While it is still not known whether Th1 or Th2 cells predominate in these lesions, it has been reported that different APCs may induce activation of different T-cell subsets. An immunoperoxidase technique was used to investigate the presence of CD1a+, CMRF-44+, CMRF-58+ and CD83+ dendritic cells, CD14+ macrophages or dendritic cell precursors and CD19+ B cells in gingival biopsies from 21 healthy or gingivitis and 25 periodontitis subjects. The samples were divided into three groups according to the size of infiltrate (group 1, small infiltrates; group 2, medium infiltrates; group 3, extensive infiltrates). The presence of numerous CD1a+ Langerhans cells was noted in the epithelium with no differences between the healthy/gingivitis and periodontitis groups. The percentage of CD83+ dendritic cells in the infiltrates was higher than the percentage of CD1a+, CMRF-44+ or CMRF-58+ dendritic cells. Endothelial cells positive for CD83 were found predominantly in areas adjacent to infiltrating cells, CD83+ dendritic cells being noted in the region of CD83+ endothelium. The percentage of CD14+ cells in the inflammatory infiltrates was similar to that of CD83+ dendritic cells. B cells were the predominant APC in group 2 and 3 tissues. The percentage of B cells in group 3 periodontitis lesions was increased in comparison with group 1 periodontitis tissues and also in comparison with group 3 healthy/gingivitis sections. Functional studies are required to determine the roles of different APC subpopulations in periodontal disease.
authors.affiliation: Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane, Australia.
authors.forename: E
authors.initials: E
authors.lastname: Gemmell
authors.forename: C L
authors.initials: CL
authors.lastname: Carter
authors.forename: D N J
authors.initials: DN
authors.lastname: Hart
authors.forename: K E
authors.initials: KE
authors.lastname: Drysdale
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
mesh_terms: D017951:Antigen Presentation / Q000276:immunology; D000938:Antigen-Presenting Cells / Q000145:classification* / Q000276:immunology; D015703:Antigens, CD / Q000032:analysis; D018949:Antigens, CD1 / Q000032:analysis; D018941:Antigens, CD19 / Q000032:analysis; D000943:Antigens, Differentiation / Q000032:analysis; D001402:B-Lymphocytes / Q000145:classification / Q000276:immunology; D003713:Dendritic Cells / Q000145:classification / Q000276:immunology; D004727:Endothelium / Q000276:immunology; D004848:Epithelium / Q000276:immunology; D005881:Gingiva / Q000276:immunology; D005891:Gingivitis / Q000276:immunology; D006801:Humans; D007124:Immunoenzyme Techniques; D007136:Immunoglobulins / Q000032:analysis; D007801:Langerhans Cells / Q000145:classification / Q000276:immunology; D016014:Linear Models; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008264:Macrophages / Q000145:classification / Q000276:immunology; D008562:Membrane Glycoproteins / Q000032:analysis; D015999:Multivariate Analysis; D010518:Periodontitis / Q000276:immunology* / Q000473:pathology; D013223:Statistics as Topic; D016176:T-Lymphocyte Subsets / Q000276:immunology; D000097802:CD83 Antigen
chemical_list: D015703:Antigens, CD; D018949:Antigens, CD1; D018941:Antigens, CD19; D000943:Antigens, Differentiation; D007136:Immunoglobulins; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D000097802:CD83 Antigen; C419393:CD1a antigen