2010 Fiscal Year Final Research Report
CEACAM1 regulates the cytokine network in intestinal mucosa
| Project/Area Number |
20590737
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
NAGAISHI Takashi Tokyo Medical and Dental University, 医学部附属病院, 助教 (60447464)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAMURA Tetsuya 東京医科歯科大学, 大学院・医歯学総合研究科, 寄附講座教員 (70265809)
TSUCHIYA Kiichiro 東京医科歯科大学, 医学部附属病院, 講師 (40376786)
WATANABE Mamoru 東京医科歯科大学, 大学院・医歯学総合研究科, 教授 (10175127)
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| Project Period (FY) |
2008 – 2010
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| Keywords | CEACAM1 / リンパ球 / 粘膜免疫 / サイトカイン / シグナル伝達 |
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| Research Abstract |
Inflammatory Bowel Disease (IBD) is characterized by unrestrained lymphocyte activation that results in the production of a variety of pro-inflammatory cytokines and other mediators. Understanding the mechanisms of lymphocyte regulation is therefore of significant importance to dysregulated mucosal inflammation such as IBD. An area that is of significant interest is the cell autonomous mechanisms of T cell regulation through proteins that have natural inhibitory functions when expressed on T lymphocytes. In this regard, we have observed that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) has the general property of negatively regulating T cell responses that are initiated by antigen/MHC complex-mediated signals. Moreover, we have demonstrated that this is clinically relevant, as CEACAM1 functions in the suppression of an IBD model. Defining the mechanisms of CEACAM1-mediated T cell regulation will lead to a significant understanding of the manner in which manipulation of this molecule may provide insights into novel therapeutic methods for the treatment of IBD.
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