The investigation of regulatory mechanisms for innate allergy by IL4-induced NK cells
| Project/Area Number |
17K15737
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Institute of Physical and Chemical Research |
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Principal Investigator |
Kiniwa Tsuyoshi 国立研究開発法人理化学研究所, 生命医科学研究センター, 基礎科学特別研究員 (90793795)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | NK cell / ILC2 / TFH / IL-4 / Allergy / IL-12 / IL-4誘導性NK細胞 / 細胞傷害活性 / 免疫学 / アレルギー・免疫関連疾患 / 2型自然リンパ球 / NK細胞 / Interleukin-4 |
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| Outline of Final Research Achievements |
In this study, we investigated the physiological roles of IL-4 induced NK cell (IL4-NK) in allergic diseases using mouse model of asthma. Especially, we focused on the interactions among T follicular helper (TFH), Group 2 innate lymphoid cells (ILC2), and IL4-NK. We found that serum IgE was reduced by injecting a depleting antibody against NK cells into asthmatic mice. Because IgE is induced by IL-4 from TFH, this result suggested that NK cell can suppress TFH during asthmatic diseases. Furthermore, we revealed that ILC2 co-cultured with IL4-NK showed lower proliferation and cytokine production compared to without IL4-NK, suggesting that IL4-NK can suppressed ILC2 directly.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究によって、アレルギー病態における新たなNK細胞の制御機構およびその生理的役割として、IL-4を受け取ったNK細胞が活性化し、TFHやILC2と相互作用しそれらを抑制することでアレルギー性炎症の過剰な亢進を抑制する、ネガティブフィードバック機構に働く可能性があることが明らかになった。IL4-NKの誘導機序やTFHおよびILC2を抑制する機構の詳細は今の所不明であるが、今後その詳細が明らかとなれば、あらたなアレルギー性疾患の治療法開発の糸口となることが期待できる。
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Report
(3 results)
Research Products
(2 results)
