| Project/Area Number |
17H06630
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Ishii Takashi 東京大学, 保健・健康推進本部, 助教 (30803118)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 気管支喘息 / アレルギー / 自然リンパ球 / ２型自然リンパ球 / 自然免疫 / 呼吸器疾患 / アレルギー疾患 / アレルギー・ぜんそく / 免疫学 |
|---|
| Outline of Final Research Achievements |
Type 2 Innate lymphoid cells (ILC2s) are known to be involved in allergic diseases such as asthma. How ILC2s are activated has been studied recently, and we focused on whether innate immune receptor TLR2 could activate ILC2s.
Upon stimulation of lung ILC2s by TLR2 agonist, allergic mediators such as IL-5 and IL-13 could be produced. Furthermore, house dust mite extract, which often causes allergic diseases, could enhance these effects. Taken together with in vivo results, Activation of lung ILC2s by TLR2 may be involved in the pathogenesis of asthma,
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| Academic Significance and Societal Importance of the Research Achievements |
２型自然リンパ球(ILC2)が自然免疫受容体のTLR2により直接的に活性化され、気管支喘息の病態、感染の後の喘息症状の悪化などに関わる可能性がある事を示した。感染時の防御反応としてTLR2を含めた自然免疫受容体の役割は重要であるが、その過剰な活性化を抑制する事で喘息症状の改善に関与できる可能性を示した。
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