| Project/Area Number |
13670898
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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 |
Dermatology
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| Research Institution | Kyorin University |
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Principal Investigator |
KANO Yoko Kyorin University, School of Medicine, Assistant Professor, 医学部, 助教授 (20142416)
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| Co-Investigator(Kenkyū-buntansha) |
TERAKI Yuichi Kyorin University, School of Medicine, Lecturer, 医学部, 講師 (10188667)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | DIHS / Severe drug eruption / CD8+T cell / Virus / Drug-lymphocyte stimulation test / IgM / IL-15Rβ / CD8^+T細胞 / リンパ球刺激実験 / 薬疹 / カルバマゼピン / CD19 / CD56 |
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| Research Abstract |
1) We have analyzed numbers of circulating lymphocytes and NK cells in patients with drug-induced hypersensitivy syndrome (DIHS) in the first year. Circulating CD19+B cells were markedly decreased in number, in patients with DIHS at the onset. This decrease was rarely noted in patients who were taking anticonvulsants without any adverse reactions (control patients). Circulating CD56+ cells were also decreased in number, in patients with DIHS at the onset but not in the control patients. These results suggested that the in number, in patients with DIHS at the onset but not in the control patients. These results suggested that the drug-induced immunological alterations might contribute to reactivation of HHV-6 in patients with DIHS.
2) Association between reactivation of HHV-6 and drug allergy were analyzed in the second year. Results of drug-lymphocyte stimulation test (DLST) were negative in patients with DIHS at the onset. However; DLST were positive at the complete recovery stage, suggesting association between DLST positivity and the decreased number of CD19+ cells. Expression of CD122 on CD56+ cells was significantly lower not only at the onset but also at the complete recovery stage in patients with DIHS. This suggests that CD56+ cells in patients with DIHS appeared not to be susceptible to stimulation through IL-15. Disturbance of CD56+ cells might be in part responsible for the stimulation of CD8+ cells, suggesting the development of DIHS.
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