Regulation of semaphorin molecules in development of colitis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25860357
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Immunology
• Research Institution: Osaka University
• Principal Investigator: Kang Sujin 大阪大学, 医学(系)研究科(研究院), 寄附講座助教 (30644398)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: semaphorin / colitis

Outline of Final Research Achievements

Type I Innate lymphoid cells (ILCs) play an important roles in maintenance of intestinal homeostasis. In this study, we identified Sema4A, which is highly expressed in innate lymphoid cells is required for type I ILC activation. Using dextran-sodium induced mouse model, we found that Sema4A deficient mice showed enhanced body weight loss and shortening of colon length from day 5 on. In addition, Sema4A was preferentially expressed in CD8+ T cells in large intestine. Deletion of Sema4A restrained expression of effector molecules such as granzyme B, perfolin and FAS, resulting in susceptible for Listeria sp. infection. Our data demonstrated that Sema4A is essential to prevent excessive intestinal inflammation and for host defense for bacterial infection.

Free Research Field

基礎医学