Functional analysis of the newly identified macrophage differentiation-inducing factor IL-32
Project/Area Number |
26461407
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Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hematology
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Research Institution | Kumamoto University |
Principal Investigator |
Suzu Shinya 熊本大学, エイズ学研究センター, 教授 (80363513)
|
Co-Investigator(Renkei-kenkyūsha) |
Noyori Osamu 熊本大学, エイズ学研究センター/国際先端医学研究拠点施設, 特定事業研究員 (30737151)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 細胞分化 / マクロファージ / サイトカイン / IL-32 / 分化 / M-CSF |
Outline of Final Research Achievements |
M-CSF stimulates differentiation/survival of macrophages (MF) and induces anti-inflammatory M2 but not pro-inflammatory M1 MF. Recently, another cytokine IL-32 was reported to promote MF differentiation. Here, we found that M-CSF has additive/inhibitory effects on IL-32 activities. When added to M-CSF-MF, these cytokines supported MF survival, which was enhanced by their combination. However, they had opposed effects on HIV-1 replication; stimulated by M-CSF and inhibited by IL-32. Anti-HIV-1 activity of IL-32 was cancelled by M-CSF. Such effect of M-CSF was not seen with IL-32-induced M1-like features including high cytokine/chemokine production and CD80 expression. Of interest, IL-32-treated MF showed also M2-like features including high phagocytosis and expression of CD14 and CD163, the latter of which was up-regulated by combination with M-CSF. Our findings help to further understand the mechanisms regulating HIV-1 replication in MF, and the survival and M1/M2 ratio of MF.
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Report
(4 results)
Research Products
(6 results)
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[Journal Article] MPL activation directly induces fibrocyte differentiation to cause myelofibrosis2017
Author(s)
Maekawa T, Osawa Y, Izumi T, Nagao S, Takano K, Okada Y, Tachi N, Teramoto M, Kawamura T, Horiuchi T, Saga R, Kato S, Yamamura T, Watanabe J, Kobayashi A, Kobayashi S, Sato K, Hashimoto M, Suzu S, Kimura F
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Journal Title
Leukemia
Volume: 印刷中
Issue: 12
Pages: 2709-2716
DOI
Related Report
Peer Reviewed
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[Journal Article] Potential role of the formation of tunneling nanotubes in HIV-1 spread in macrophages.2016
Author(s)
Hashimoto M, Bhuyan F, Hiyoshi M, Noyori O, Nasser H, Miyazaki M, Saito T, Kondoh Y, Osada H, Kimura S, Hase K, Ohno H, Suzu S
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Journal Title
J Immunol
Volume: 196
Issue: 4
Pages: 1832-1841
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Fibrocytes differ from macrophages but can be infected with HIV-1.2015
Author(s)
M. Hashimoto, H. Nasser, F. Bhuyan, N. Kuse, Y. Satou, S. Harada, K. Yoshimura, J. Sakuragi, K. Monde, Y. Maeda, S. Welbourn, K. Strebel, E.W.A. El-Wahab, M. Miyazaki , S. Hattori, N. Chutiwitoonchai, M. Hiyoshi, S. Oka, M. Takiguchi, S. Suzu.
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Journal Title
The Journal of Immunology
Volume: 195
Issue: 9
Pages: 4341-4350
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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