Identification of a novel role for innate immune sensor NLRP
| Project/Area Number |
23590327
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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 |
General medical chemistry
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 細胞内シグナル伝達 / がん / シグナル伝達 / 免疫 |
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| Research Abstract |
The nucleotide-binding oligomerization domain-like receptors (NLR ) family member NLRP3 is a central regulator of innate immunity. We recently found that NLRP3 mediates NF-kappaB activation and cytokine transcription in human monocytic cell line THP-1 following microbial infection. In this study, we examined the effect of NLRP3 knockdown on cytokine induction following sterile stimulation to clarify the physiological relevance of this function. NLRP3 knockdown reduced cytokine induction in THP-1 and human monocytes following sterile stimulation. Next, we examined the role of NLRP3 in tumor cell lines. NLRP3 knockdown reduced the constitutive expression of IL-1beta in these tumor cell lines. Interestingly, the expression of TGF-beta, IL-6, and matrix metalloproteinase were reduced in knockdown cells. These data suggest that NLRP3 not only mediates cytokine transcription for innate immunity but also contributes tumor progression through the induction of tumor-related gene expression.
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Report
(4 results)
Research Products
(8 results)
