Analysis of the mechanisms of pathogenesis and eradication response in Helicobacter pylori-associated immune thrombocytopenia
| Project/Area Number |
26870561
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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 |
Hematology
Laboratory medicine
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| Research Institution | Kitasato University |
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Principal Investigator |
SATOH Takashi 北里大学, 医療衛生学部, 講師 (90407114)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
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)
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| Keywords | 免疫性血小板減少症 / Helicobacter pylori / H.pylori / Fcγ受容体 / SNP |
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| Outline of Final Research Achievements |
In this study, the associations between gene polymorphisms and rates of Helicobacter pylori (H. pylori) eradication response in patients with H.pylori-associated immune thrombocytopenia (ITP) were evaluated. Patients with ITP who were carriers of the FcγRIIB 232T or TGF-β -509T polymorphisms had significantly higher rates of H. pylori eradication responses than non-carriers. The frequency of the circulating anti-glycoprotein IIb/IIIa antibody-producing cells was significantly higher in patients with ITP that carried the FcγRIIB 232T allele than in those with the non-T allele. In addition, patients with ITP that carried the TGF-β -509T allele tended to have lower TGF-β levels. These findings suggest that FcγRIIB 232I/T and TGF-β -509C/T gene polymorphisms contribute to the susceptibility of H.pylori-associated ITP by controlling the autoimmune responses.
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Report
(3 results)
Research Products
(1 results)
