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Published online before print June 16, 2003
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chains by human gingival fibroblasts and up-regulation of adhesion to neutrophils in response to IL-2





Departments of
* Microbiology and Immunology and
Periodontics and Endodontics, Tohoku University Graduate School of Dentistry, and
Department of Animal Production Science, Tohoku University Graduate School of Agricultural Science, Sendai, Japan
1Correspondence: Department of Microbiology and Immunology, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan. E-mail: sugawars{at}mail.cc.tohoku.ac.jp
To investigate the role of human gingival fibroblasts (HGF), the major constituents of gingival tissue in periodontal inflammatory disease, the expression of interleukin-2 receptor (IL-2R)
, ß, and
chains was examined. Immunohistochemistry showed a pronounced accumulation of CD8+ T cells in the inflamed lamina propria of gingival tissue from patients with adult periodontitis. HGF express IL-2Rß and IL-2R
at mRNA and protein levels, but the expression of IL-2R
could not be detected, as assessed by reverse transcriptase-polymerase chain reaction and flow cytometry. IL-2Rß, and -
expressed on HGF were functionally active, as addition of neutralizing anti-IL-2Rß and -
antibodies caused inhibition of the IL-2-induced production of monocyte chemoattractant protein-1 (MCP-1), and addition of IL-2 induced phosphorylation of Janus tyrosine kinase 3, which is critical in signaling through IL-2R
in HGF. The IL-2-induced MCP-1 production was significantly inhibited by pretreatment with neutralizing antibody to IL-15. Addition of IL-2 also induced a marked up-regulation of the expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of HGF, which in turn, significantly augmented the adhesion of human neutrophils, which were inhibited by an anti-ICAM-1 antibody. These results suggest that HGF express functional IL-2Rß
, respond to IL-2 from infiltrated T cells, and actively participate in the inflammatory process in the periodontal region and that IL-15 produced by HGF sustains IL-2-mediated signaling in HGF.
Key Words: gingival tissue cytokine receptor chemokine adhesion molecule periodontitis
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