Identification of memory Th2 stem cells that control allergic reactions
| Project/Area Number |
20590485
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Chiba University |
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Principal Investigator |
YAMASHITA Masakatsu Chiba University, ゲノム医学研究室, 室長 (00311605)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | アレルギー / Th2細胞 / 免疫記憶 / メモリーT細胞 / サイトカイン / メモリーTh細胞 / 転写因子 / 幹細胞 |
|---|
| Research Abstract |
We show that memory Th2 cells are subdivided into at least four subpopulations by CD62L and CXCR3 expression. All four subpopulations produced IL-4 and IL-13 upon TCR-mediated re-stimulation, while only CD62L-low/CXCR3-low population produced IL-5. We performed a DNA microarray analysis and found that CD62L-low/CXCR3-low subpopulation expressed osteopontin, IL-6, and IL-10. We speculate that CD62L-low/CXCR3-low memory Th2 cells may therapeutic target for allergic disorders. We screened low molecular weight compounds and found that synthetic thioamide-related compound SH-2251 inhibited the generation of IL-5 producing memory Th2 cells as well as IL-5 production. Furthermore, SH-2251 also inhibited osteopontin, IL-6, and IL-10 expression. These results indicate that SH-2251 may modulateCD62L-low/CXCR3-low memory Th2 cell functions.
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Report
(4 results)
Research Products
(58 results)
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[Journal Article] Polycomb group gene product Ring1B regulates Th2-driven airway inflammation through the inhibition of Bim-mediated apoptosis of effector Th2 cells in the lung.2010
Author(s)
Suzuki A., Iwamura C., Shinoda K., Tumes JD., Kimura YM., Hosokawa H., Endo Y., Horiuchi S,, Tokoyoda K., Koseki H., Yamashita M., Nakayama T.
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Journal Title
J.Immunol. 184
Pages: 4510-4520
Related Report
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[Journal Article] CD69 controls the pathogenesis of allergic airway inflammation.2009
Author(s)
Miki HT., Hasegawa A., Iwamura C., Shinoda K, Tofukuji S., Watanabe Y., Hosokawa H., Motohashi S., Hashimoto K., Shirai M., Yamashita M., Nakayama T.
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Journal Title
J.Immunol. 183
Pages: 8203-8215
Related Report
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[Journal Article] Enhanced Th2 cell differentiation and allergen-induced airway inflammation in Zfp35-deficient mice.2009
Author(s)
Kitajima M., Iwamura C., Miki HT., Shinoda K., Endo Y. Watanabe Y., Shinnakasu R., Hosokawa H., Hashimoto K., Motohashi S., Koseki H., Ohara O., Yamashita M., Nakayama T.
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Journal Title
J.Immunol. 183
Pages: 5388-5396
Related Report
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[Journal Article] ROG, repressor of GATA, regulates Th2-driven allergic airway inflammation and airway hyperresponsiveness.2008
Author(s)
Hirahara K., Yamashita M., Iwamura C., Shinoda K., Hasegawa A., Yoshizawa H., Koseki H., Gejyo F., Nakayama T.
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Journal Title
J.Allergy Clin.Immunol. 122
Related Report
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[Journal Article] Human Th1 differentiation induced by lipoarabinomannan/lipomannan from Mycobacterium bovis BCG Tokyo-172.2008
Author(s)
Ito T., Hasegawa A., Hosokawa H., Yamashita M., Motohashi S., Naka T., Okamoto Y., Fujita,Y., Ishii Y., Taniguchi M., Yano I., Nakayama T.
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Journal Title
Int.Immunol. 20
Pages: 849-860
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