title: CXCL13 expression and follicular dendritic cells in relation to B-cell infiltration in periodontal disease tissues.
abstract: OBJECTIVE
  B lymphocyte is the dominant infiltrating cell type in periodontitis lesions. CXCL13, produced by follicular dendritic cells, endothelial cells and fibroblasts, is crucial for B-cell trafficking. An association between chronic inflammation and lymphoid organogenesis has been reported in infection and in autoimmune responses, in which T-cell/B-cell follicles with a follicular dendritic cell network are formed. The aim of this study was to examine CXCL13 expression and follicular dendritic cell distribution in relation to B-cell infiltration in chronic inflammatory periodontal lesions.
  
  
  METHODS
  Fifty-eight gingival tissue biopsies from patients with periodontitis and 25 samples from subjects with gingivitis were analyzed. Gene expression for CXCL13 and for the CD21 long isoform was analyzed using the reverse transcription-polymerase chain reaction. Immunohistochemical analysis was performed using antibodies to CXCL13, CXCR5, follicular dendritic cells, CD3 and CD19 on serial cryostat sections.
  
  
  RESULTS
  mRNA for CXCL13 was expressed in both periodontitis and gingivitis tissues. The number of CXCL13+ cells was significantly higher in periodontitis than in gingivitis in connective tissues subjacent to the pocket epithelium and positively correlated with the number of CD19+ cells. CXCL13+ cells were distributed in B-cell-dominant areas both with and without follicular dendritic cells. Although obvious reticular networks of follicular dendritic cells were not found in periodontitis and gingivitis, the accumulation of follicular dendritic cells in B-cell-dominant areas in periodontitis was observed in some patients.
  
  
  CONCLUSIONS
  These findings suggested that CXCL13 and follicular dendritic cells were involved in B-cell recruitment to, and B-cell distribution in, chronic inflammatory periodontal lesions.
authors.affiliation: General Dentistry and Clinical Education Unit, Niigata University Medical and Dental Hospital, Niigata, Japan. takako@dent.niigata-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: R
authors.initials: R
authors.lastname: Amanuma
authors.forename: K
authors.initials: K
authors.lastname: Ueki-Maruyama
authors.forename: T
authors.initials: T
authors.lastname: Oda
authors.forename: T
authors.initials: T
authors.lastname: Honda
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D018941:Antigens, CD19 / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000502:physiology*; D002465:Cell Movement; D054382:Chemokine CXCL13 / Q000096:biosynthesis*; D055113:Chronic Periodontitis / Q000276:immunology* / Q000378:metabolism; D020566:Dendritic Cells, Follicular / Q000378:metabolism*; D015870:Gene Expression; D005891:Gingivitis / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007124:Immunoenzyme Techniques; D008875:Middle Aged; D054380:Receptors, CXCR5 / Q000096:biosynthesis; D017464:Receptors, Complement 3d / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D018941:Antigens, CD19; C110663:CXCL13 protein, human; C095085:CXCR5 protein, human; D054382:Chemokine CXCL13; D054380:Receptors, CXCR5; D017464:Receptors, Complement 3d