| Project/Area Number |
24591471
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKANO Yasuko 昭和大学, 薬学部, 教授 (20155790)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 制御性T細胞 / カルシウム / RACK1 / 酸化ストレス / ペルオキシレドキシン / ERK / 国際情報交換 / イギリス：スペイン / アレルギー疾患 / カルシウムチャネル / カルシウムイオン / 免疫抑制 / CRACチャネル / イギリス：スペイン：アメリカ |
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| Outline of Final Research Achievements |
One of the asthma pathologies is a persistent inflammation in airway caused by allergens and viruses. The impaired functions and decreased number of regulatory T cells (Tregs) is considered as the cause of persistent inflammation in local sites. The mechanisms of abnormal functions of Tregs are obscure. Therefore, the aim of this study was to analyze the functions of Tregs by using Ca2+ response against T cell receptor stimulation, which can estimate the regulatory functions of Tregs, and to elucidate the mechanisms of abnormal functions of Tregs. The results showed that increasing Ca2+ response in Tregs from patients with asthma was attributed to the increasing expression of scaffold protein, RACK1. In addition, the new data associated with the abnormal functions of Tregs was obtained from microarray analysis.
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