Upregulation of co-stimulatory molecule expression and dendritic cell marker (CD83) on B cells in periodontal disease.
T cells and their cytokines are well known for their important role in the pathogenesis of periodontitis. To date, the role of antigen presenting cells (APCs), which are known to be critical in the regulation of T cell response, has been poorly investigated in periodontitis. In this study, we analyzed the expression of co-stimulatory molecules (CD80 and CD86) and CD83, which is a marker of mature dendritic cells, on gingival cells that were isolated from severe periodontitis tissues, with the use of flow cytometry. Significant upregulation of CD86 and CD83 expression was detected in periodontitis lesions, and most of this occurred on B cells. In vitro peripheral blood mononuclear cell cultures showed that stimulation with different periodontopathic bacteria, that included Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, and Actinomyces viscosus, upregulated both CD86 and CD83 expression on B cells. Therefore, the presence of plaque bacteria may be responsible for the enhanced expression seen in vivo on gingival B cells. APC function by bacterial-activated B cells was further investigated using allogeneic mixed leukocyte reactions. After 24 h culture with either A. actinomycetemcomitans or P. gingivalis, these activated B cells performed as potent APCs in mixed leukocyte reactions, and they stimulated T cells to produce high levels of gamma interferon and minimal interleukin-5. In conclusion, periodontopathic bacterial-induced B cell activation with upregulation of CD86 and CD83 may be associated with enhanced APC function. The results of this study suggest, therefore, that infiltrated gingival B cells have a possible role as APCs in the regulation and maintenance of local T cell response in periodontitis.
Mahanonda
Rangsini
R
Department of Periodontology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand. mrangsin@chula.ac.th
Sa-Ard-Iam
Noppadol
N
Yongvanitchit
Kosol
K
Wisetchang
Mahisorn
M
Ishikawa
Isao
I
Nagasawa
Toshiyuki
T
Walsh
Douglas S
DS
Pichyangkul
Sathit
S
D000328:Adult; D000938:Antigen-Presenting Cells / Q000276:immunology*; D015703:Antigens, CD / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000276:immunology*; D018122:B7-1 Antigen / Q000096:biosynthesis; D051940:B7-2 Antigen; D001421:Bacteria, Anaerobic / Q000276:immunology / Q000472:pathogenicity*; D002478:Cells, Cultured; D003773:Dental Plaque / Q000382:microbiology; D005434:Flow Cytometry; D005881:Gingiva / Q000166:cytology / Q000276:immunology; D006801:Humans; D007136:Immunoglobulins / Q000096:biosynthesis; D007156:Immunologic Memory; D007371:Interferon-gamma / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology*; D013601:T-Lymphocytes / Q000378:metabolism; D015854:Up-Regulation; D000097802:CD83 Antigen
D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D007136:Immunoglobulins; D007371:Interferon-gamma; D015848:Interleukin-5; D008562:Membrane Glycoproteins; D000097802:CD83 Antigen; C497964:CD86 protein, human