2016 Fiscal Year Final Research Report
Functional mechanism of IVIG and cyclosporin A therapy for IVIG-resistant Kawasaki disease
| Project/Area Number |
26860821
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 川崎病 / シクロスポリンA / 細胞内シグナル伝達 |
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| Outline of Final Research Achievements |
Peripheral blood samples were obtained just before and after the initial course of IVIG, additional IVIG, and CsA therapy for patients with Kawasaki disease. To evaluate the NFAT pathway and activation of the JAK-STAT pathway, we examined the gene expression of cytokines and intracellular signal transducers using real-time RT-PCR and pSTAT3 and pSTAT5 using flow cytometry. In the CsA group, expression of mRNAs for NFATc1 and c2 was significantly increased, whereas the mean fluorescence intensity (MFI) of pSTAT3 was decreased after CsA treatment. In the group responsive to initial IVIG, the MFI of pSTAT3 was decreased, and that of pSTAT5 was increased, after IVIG. In patients with refractory KD, CsA exerts effects on the activity of the JAK-STAT pathways and NFAT pathway.
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| Free Research Field |
小児循環器学
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