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- Inoue Hiroshi
- Department of Physiology, Osaka Dental University
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- Goda Seiji
- Department of Biochemistry, Osaka Dental University
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- Domae Naochika
- Department of Internal Medicine, Osaka Dental University
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- Nosaka Ko
- Department of Physiology, Osaka Dental University
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- Nakai Masanori
- Department of Physiology, Osaka Dental University
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- Uchihashi Kenji
- Department of Physiology, Osaka Dental University
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- Nishikawa Yasuo
- Department of Physiology, Osaka Dental University
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抄録
Natural killer (NK) cells play a key role in inflammation and tumor regression through their ability to migrate into tissues. The two major subsets in NK cells are CD56bright CD16dim/- and CD56dim CD16+. The cytotoxic activity of CD56dim NK cells is significantly greater than that of CD56bright cells. Regarding cytokine production, the situation is inverted. CD56bright NK cells are the most efficient cytokine producers. The role of CD56bright CD16- cells is not clear. CXCL12 is a chemokine that promotes Iymphocyte invasion and migration into tissues; however, the mechanism for this process remains incompletely understood. This study demonstrated that the NK92 cell population, which is the human NK cell line, was CD56bright CD16-. We examined the production of pro-matrix metalloproteinase (MMP) 1 induced by CXCL12 stimulation on NK92 cells. Pro-MMP 1 production was significantly enhanced by CXCL12 stimulation. In addition, the production of pro-MMP 1 was markedly inhibited by SB203580 (p38 inhibitor). These results suggest that p38, which is the family of mitogen activated protein kinases (MAPKs), was involved in the production of pro-MMP 1 from CXCL12-stimulated CD56bright CD16- NK92 cells.
収録刊行物
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- Journal of Osaka Dental University
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Journal of Osaka Dental University 43 (2), 163-167, 2009
大阪歯科学会
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詳細情報 詳細情報について
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- CRID
- 1390282679938572800
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- NII論文ID
- 110007386259
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- NII書誌ID
- AA00704144
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- ISSN
- 21896488
- 04752058
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可