2015 Fiscal Year Final Research Report
The Pathogenesis of Autoimmune Hemorrhaphilia XIII/13: Analysis of Anti-FXIII/13 Autoantibodies and Elucidation of Their Generation Mechanisms
| Project/Area Number |
25461444
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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 |
Hematology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SOURI Masayoshi 山形大学, 医学部, 准教授 (20292419)
OSAKI Tsukasa 山形大学, 医学部, 助教 (60380565)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 自己免疫性出血病 / 高齢化社会 / 慢性難治性弛緩 / 分子病態 / 自己抗体 / エピトープ解析 / ユニバーサルエピトープ / 質量分析 |
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| Outline of Final Research Achievements |
1. Types of anti-factor 13 (F13) autoantibodies: 1) Among 15 autoimmune hemorrhaphilia 13 (AH13) cases, 10 patients had Aa type, one had B type, and the remaining 4 cases had both types. 2) After recombinant F13 A subunit (F13-A) was digested with proteases in the presence or absence of patient’s plasma, their autoantibodies’ epitopes were mapped by compering the amounts of digested peptides (through protection of digestion). It was suggested that F13 activation by thrombin might be inhibited by binding of these antibodies, especially by Aa type.
2. Genetic backgrounds for autoantibody generation: 1) By analyzing the whole exome sequences for the F13-A gene of 6 Aa- and two Ab-type patients, a possibility that its genetic polymorphisms result in differential antigenicity was suggested. 2) When immune response related genes such as CTLA-4 and HLA class II were analyzed, their genetic polymorphisms did not show any tendency toward production of autoantibodies against the F13-A protein.
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| Free Research Field |
血液内科学
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