| Project/Area Number |
18390152
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Osaka University |
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Principal Investigator |
KUMANOGOH Atsushi Osaka University, Research Institute for Microbial Diseases, Professor (10294125)
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| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥16,500,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2007: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2006: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | helper T-cells / semaphorin / atopic dermatitis / autoimmune diseases / autoimmune cardiotitis |
|---|
| Research Abstract |
Semaphorins have been identified as axon guidance factors during neuronal development. Recently, our cumulative findings indicate that several semaphorins are crucially involved in distinct phases of immune responses. Sema4A is a classIV semaphroin member and is shown to be important for T-cell activation. Here, we have found that Sema4A is crucially relevant to Th1/Th2 regulation. Actually, Sema4A-deficient mice exhibited reduced Th1 but rather enhanced Th2 responses. In addition, the mutant mice spontaneously develop atopic dermatitis, in which recombinant Sema4A proteins ameliorated the severity of the dermatitis. Collectively, our findings not only clarify the importance of Sema4A in helper T-cell differentiation but also provide a potential therapeutic target for treating immunological disorders including allergic and autoimmune diseases.
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