title: Expression of the cutaneous lymphocyte antigen and the alpha IEL beta 7 integrin by intraepithelial lymphocytes in healthy and diseased human gingiva.
abstract: The presence of specific phenotypes of intraepithelial lymphocytes (IEL) was determined in healthy and diseased gingiva by immunohistochemistry. The cutaneous lymphocyte antigen (CLA) and the alpha IEL beta 7 integrin were detected with the HECA-452 and with the HML-1 monoclonal antibodies, respectively. Some 24-62% of CD3-positive intraepithelial lymphocytes expressed the CLA antigen in the junctional epithelium, while 49-54% expressed the alpha IEL beta 7 integrin. Similar results were obtained in the other gingival epithelia. The fraction of CLA-positive T cells and alpha IEL beta 7 integrin-positive T cells was significantly higher in the gingival epithelia than in the underlying connective tissue, indicating that the T-cell subsets defined by these surface adhesion molecules were selectively localized in the epithelial compartment. Comparison of the fractions of CLA-positive and alpha IEL beta 7 integrin-positive T cells across different disease groups did not show significant differences. The data indicate that intraepithelial lymphocytes expressing the CLA and the alpha IEL beta 7 phenotype are a quantitatively important component of gingival intraepithelial immunity. These adhesion molecules may play a part in the retention of specific T-cell subsets in gingival epithelia.
authors.affiliation: Department of Periodontology and Fixed Prosthodontics, University of Bern, Switzerland.
authors.forename: M S
authors.initials: MS
authors.lastname: Tonetti
authors.forename: A M
authors.initials: AM
authors.lastname: Straub
authors.forename: N P
authors.initials: NP
authors.lastname: Lang
mesh_terms: D000328:Adult; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm / Q000032:analysis* / Q000235:genetics; D014408:Biomarkers, Tumor / Q000032:analysis* / Q000235:genetics; D003238:Connective Tissue / Q000276:immunology / Q000473:pathology; D015921:Dental Implants; D004848:Epithelium / Q000276:immunology / Q000473:pathology; D005786:Gene Expression Regulation; D005881:Gingiva / Q000276:immunology* / Q000473:pathology; D005891:Gingivitis / Q000276:immunology* / Q000473:pathology; D006801:Humans; D016023:Integrins / Q000032:analysis* / Q000235:genetics; D008562:Membrane Glycoproteins / Q000032:analysis* / Q000235:genetics; D010518:Periodontitis / Q000276:immunology / Q000473:pathology / Q000628:therapy; D010641:Phenotype; D011565:Psoriasis / Q000276:immunology / Q000473:pathology; D016201:Receptors, Lymphocyte Homing / Q000032:analysis* / Q000235:genetics; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000473:pathology
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; C063419:CTAGE1 protein, human; D015921:Dental Implants; D016023:Integrins; D008562:Membrane Glycoproteins; D016201:Receptors, Lymphocyte Homing