2015 Fiscal Year Final Research Report
Analysis of the mechanism of break immune tolerance and blister formation in paraneoplastic pemphigus.
Project/Area Number |
25860976
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Dermatology
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Research Institution | Kurume University |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 腫瘍随伴性天疱瘡 / 自己抗原 / A2ML1 / エピプラキン / 免疫ブロット法 / 免疫沈降法 / 閉塞性細気管支炎 |
Outline of Final Research Achievements |
We analyzed 108 cases of paraneoplastic pemphigus (PNP) in detail. We indicated the possibility that autoantibody for A2ML1 which is newly specific autoantigen was one of the pathogenic autoantibody of PNP. Furthermore, we indicated the possibility of the autoantibody production from associated tumor. Additionally, we indicated that epiplakin (EPPK) which is a plakin protein was one of the major PNP pathogenetic autoantigens and was related to PNP-related bronchiolitis obliterans (BO). The presence of anti-EPPK antibodies was significantly related to the development of BO and higher mortality. Therefore, detection of anti-EPPK antibodies may lead to more extensive treatments to avoid the development of fatal PNP-related BO.
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Free Research Field |
皮膚科学
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