title: Increased infiltration of CD1d and natural killer T cells in periodontal disease tissues.
abstract: BACKGROUND
  Natural killer T (NKT) cells are a unique T lymphocyte subset that has been implicated in the regulation of immune responses associated with a broad range of diseases including autoimmunity, infectious diseases, and cancer. In contrast to conventional T cells, NKT cells are reactive to major histocompatibility complex (MHC) class I-like molecule CD1d. Considering the periodontitis having both aspects of infection and autoimmunity in nature, CD1d and reactive NKT cells are of particular importance.
  
  
  OBJECTIVE
  The aim of the present study was to examine whether the expression of CD1 isoforms and Valpha24(+) invariant NKT cells is associated with different disease entities, namely gingivitis and periodontitis.
  
  
  METHODS
  Immunohistochemical analysis was performed on cryostat sections of gingival tissues from 19 patients with periodontitis and eight patients with gingivitis using antibodies to CD1a, b, c, d, Valpha24(+) invariant NKT cells, CD83, CD3 and CD19.
  
  
  RESULTS
  Although all four subsets of CD1 molecules were expressed in periodontal lesions, CD1d was most abundant. CD1d expression was more frequent in periodontitis than gingivitis and increased together with increase of invariant NKT cell infiltration. Double immunohistochemical staining showed co-expression of CD1d and CD19 on identical cells and proximate infiltration of CD1d(+) and invariant NKT cells.
  
  
  CONCLUSIONS
  These findings suggest that CD1d-expressing B cells could activate NKT cells by CD1d-restricted manner and this NKT cell activation may play roles in pathogenesis of periodontal diseases.
authors.affiliation: Periodontology and Immunology, Department of Oral Health and Welfare, Niigata University Faculty of Dentistry, Niigata, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Amanuma
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: H
authors.initials: H
authors.lastname: Yoshie
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000032:analysis; D015703:Antigens, CD / Q000032:analysis; D018949:Antigens, CD1 / Q000032:analysis*; D018941:Antigens, CD19 / Q000032:analysis; D055610:Antigens, CD1d; D015551:Autoimmunity / Q000276:immunology; D017252:CD3 Complex / Q000032:analysis; D002908:Chronic Disease; D005260:Female; D005891:Gingivitis / Q000276:immunology; D006023:Glycoproteins / Q000032:analysis; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D008875:Middle Aged; D010510:Periodontal Diseases / Q000276:immunology*; D010518:Periodontitis / Q000276:immunology; D020033:Protein Isoforms / Q000032:analysis; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000032:analysis; D000097802:CD83 Antigen
chemical_list: D000469:Alkaline Phosphatase; D015703:Antigens, CD; D018949:Antigens, CD1; D018941:Antigens, CD19; D055610:Antigens, CD1d; D017252:CD3 Complex; D006023:Glycoproteins; D007136:Immunoglobulins; D008562:Membrane Glycoproteins; D020033:Protein Isoforms; D016693:Receptors, Antigen, T-Cell, alpha-beta; D000097802:CD83 Antigen; C437944:CD1C protein, human; C526877:CD1D protein, human; C419393:CD1a antigen