The roles of ILC2 and basophils on the severity of allergic conjunctivitis
Project/Area Number |
16H07189
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Single-year Grants |
Research Field |
Ophthalmology
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Research Institution | Juntendo University |
Principal Investigator |
Jobu Sugita 順天堂大学, 医学部, 助手 (90622712)
|
Project Period (FY) |
2016-08-26 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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Keywords | アレルギー性結膜炎 / 好塩基球 / 好酸球 / ILC2 / 2型炎症 / サイトカイン / 2型自然リンパ球 / 自然免疫 / 獲得免疫 |
Outline of Final Research Achievements |
We found basophil depletion in mouse papain-induced allergic conjunctivitis model induced significant suppression of eosinophil infiltration. We then found that innate lymphoid cell type2 (ILC2) depletion in mouse papain-induced allergic conjunctivitis model induced significant suppression of eosinophil infiltration. Furthermore, we found activation of ILC2 in conjunctival tissue was suppressed in allergic conjunctivitis model using IL-33 (one of the signature cytokines of type 2 immune reaction) knockout mouse. In addition, we found the existence of ILC2 in severe chronic human allergic conjunctivitis tissue (giant papillae tissue obtained from vernal keratoconjunctivitis patients) using flow cytometer (FACS).
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Report
(3 results)
Research Products
(2 results)
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[Journal Article] Contributions of Intreleukin-33 and TSLP in a papain-soaked contact lens-induced mouse conjunctival Inflammation model.2017
Author(s)
Sugita J, Asada Y , Ishida W, Iwamoto S, Sudo K, Suto H, Matsunaga T, Fukuda K, Fukushima A, Yokoi N, Ohno T, Azuma M, Ebihara N, Saito H, Kubo M, Nakae S, Matsuda A.
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Journal Title
Immunity, Inflammation and Disease.
Volume: 5(4)
Issue: 4
Pages: 515-525
DOI
Related Report
Peer Reviewed / Open Access
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