Inflammation control by novel nuclear IkB, IkBL

• Project/Area Number: 25460503
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Tokai University
• Principal Investigator: SATO Takehito 東海大学, 医学部, 准教授 (50235363)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000); Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000); Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000); Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
• Keywords: 自己免疫 / 炎症 / NFkB / IkappaBL

Outline of Final Research Achievements

Contribution to the inflammation control by I kappa B-like (IkBL) was examined. Tg mice showed reduced severity of experimentally-induced arthritis, mainly resulting from reduced function of innate immune cells such as macrophages. However, KO mice did not show significant change in the severity of acute inflammation induced by cecal ligation and puncture (CLP) or LPS injection. It is found that IkBL showed inhibitory effect on the transactivation of NFkB dependently on its nuclear translocation and that IkBL binds specifically to RelB protein, suggesting that it is involved in the control of inflammation through the modification of RelB function. Physiological significance of IkBL is to be further investigated.