This Article Abstract Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Teng, Y.-T. A. Search for Related Content PubMed PubMed Citation Social Bookmarking                         What's this?

THE ROLE OF ACQUIRED IMMUNITY AND PERIODONTAL DISEASE PROGRESSION

^* Division of Periodontics, School of Dentistry, and Department of Microbiology & Immunology, Faculty of Medicine & Dentistry, the University of Western Ontario, London, Ontario N6A 5C1, Canada; Lawson Health Research Institute, London Health Sciences Centre, London, Ontario N6A 4G5; and Division of Periodontics, Eastman Dental Clinic, Center for Oral Biology, and Dept. of Microbiology and Immunology, School of Medicine & Dentistry, University of Rochester, NY, USA 14620-2989;

View larger version (36K): [in this window] [in a new window]   Figure 1. Expression of RANK-L on A. actinomycetemcomitans-reactive periodontal CD4+ T-cells detected by flow cytometry and PCR analyses. The left panel (FACS analysis of RANK-L expression on cell surface by immunostaining to OPG-FITC conjugates): (a) un-stimulated HuPBL-derived CD4+ T-cells as background control; (b) isotypic Ig control for background staining; (c) HuPBL-derived CD4+ T-cells activated by anti-h-βTCR plus anti-CD28 Mabs as positive control for RANK-L expression; and (d) periodontal CD4+ T-cells stained with OPG-FITC for cell-surface expression of RANK-L. The right panel (RT-PCR by the use of specific primers for RANK-L): (1) A. actinomycetemcomitans (Aa)-reactive periodontal CD4+ T-cells from HuPBL-NOD/SCID mice which received HuPBL samples from one LJP subject (called LJP 2); (2) Aa-reactive periodontal CD4+ T-cells from HuPBL-NOD/SCID mice which received HuPBL samples from another LJP subject (called LJP 1); (3) naïve unstimulated HuPBL-derived CD4+ T-cells; and (4) HuPBL-derived CD4+ T-cells activated by anti-h-βTCR plus anti-CD28 mAbs as positive control for RANK-L expression. The experimental procedures have been described previously (Teng et al., 2000; Teng, 2002).

View larger version (36K): [in this window] [in a new window]   Figure 2. Interaction of CD4+ T-cells and alveolar bone remodeling in the periodontium. After being challenged by periodontal pathogens through antigen processing and presentation (via APC-dendritic cells, macrophages, activated B-cells, etc.), these micro-organisms-specific periodontal CD4+ T-cells become activated and produce RANK-L molecules. RANK-L can activate osteoclasts (OC) directly to induce bone resorption and also induce the differentiation, survival, and activation of OC precursors. OPG, the natural decoy receptor of RANK-L produced by the stromal cells (i.e., osteoblasts, chondrocytes), can compete for the binding to RANK-L molecules, thereby counteracting the effects of RANK-L/RANK signaling on OC and OC precursors.

Critical Reviews in Oral Biology & Medicine, Vol. 14, No. 4, 237-252 (2003)
DOI: 10.1177/154411130301400402


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?