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Published online before print June 16, 2003

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© 2003 by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0103044

Received for publication January 27, 2003.
Revised May 2, 2003.
Accepted for publication May 3, 2003.

Article

Expression of IL-2 receptor and chains by human gingival fibroblasts and up-regulation of adhesion to neutrophils in response to IL-2

Akiko Ozawa ^*, Hiroyuki Tada ^*, Riyoko Tamai ^*, Akiko Uehara ^*, Kouichi Watanabe , Takahiro Yamaguchi , Hidetoshi Shimauchi , Haruhiko Takada ^*, and Shunji Sugawara ^*@

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

^@ To whom correspondence should be addressed. E-mail: sugawars{at}mail.cc.tohoku.ac.jp.

	Abstract

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) , , 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-2R 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-2R, -, and - expressed on HGF were functionally active, as addition of neutralizing anti-IL-2R 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-2R, 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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