TANAKA Shigehisa Aichi-Gakuin Univ., Dept. of Periodontology, Sch. of Dent., Assistant Professor, 歯学部, 助手 (30367619)
早川 祐久 愛知学院大学, 歯学部, 講師 (00261016)
大口 将弘 愛知学院大学, 歯学部, 講師 (00319196)
|Budget Amount *help
¥3,000,000 (Direct Cost : ¥3,000,000)
Fiscal Year 2003 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 2002 : ¥600,000 (Direct Cost : ¥600,000)
Fiscal Year 2001 : ¥1,900,000 (Direct Cost : ¥1,900,000)
Interleukin-15 (IL-15) is an important cytokine which resembles IL-2 in its biological activity, stimulating macrophages, NK cells, αβ/γδ T. cells, and B cells to proliferate, secrete cytokines, exhibit increased cytotoxicities, antitumor activity, and produce antibodies (Abs). IL-15 mRNA is constitutively expressed in various cells and tissues such as placenta, skeletal muscle, kidney, epithelial cells, and macrophages. Since IL-15 expression is regulated not only at the transcriptional level but also at the translational level, IL-15 protein is found to be produced only by limited populations such as activated monocytes/macrophages and epithelial cells. Furthermore, IL-15 is involved in an etiology of rheumatoid arthritis.
We previously reported that exogenous IL-15 preferentially stimulated intestinal intraepithelial lymphocytes (i-IEL) to proliferate and produce interferon-y (IFN-γ). It was reported elsewhere that i-EC constitutively expressed IL-15 mRNA and produced IL-15 protein.
Taken together, it appears that IL-15 produced by i-EC is an important mediator in the intestinal immune system that serves as a primary immune barrier against microbial invasion. Consequently, we monitored i-IEL and intestinal epithelial cells (i-EC) in mice after an oral infection with Listeria monocytogenes, and found that IL-15 was produced by i-EC at an early stage after the oral infection with L. monocyto genes, and concurrently the i-IEL were activated to produce IFN-γ.
In this study, to determine whether cytokine derived from epithelial cell is involved in activation of T cells during gingival infection as an etiology of periodontal disease, we monitored KB cells and T cells after stimulation with lipopolysaccharide (LPS). IL-15 expression in KB cells treatment with ricombinant human IFN-γ was increased by LPS. Moreover, T cell proliferation was increased by culture supernatants from LPS stimulated KB cell, but not without LPS stimulation. These results suggested that IL-15 produced from KB cells may be at least partly involved in the activation of T cells after stimulation with LPS. Less