2015 Fiscal Year Final Research Report
Genotype identification of RA and SLE using Fc gamma RIIB-deficient B6 mice.
| Project/Area Number |
25461486
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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 |
Collagenous pathology/Allergology
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HIROSE Sachiko 順天堂大学, 医学部, 准教授 (00127127)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 全身性エリテマトーデス / 疾患モデルマウス |
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| Outline of Final Research Achievements |
Background: FcγRIIB negatively regulates BCR-mediated activation signals. We used FcγRIIB-deficient B6-congenic mouse strain (KO1) spontaneously developed pathology of rheumatoid arthritis (RA). Methods: To analyse the phenotypic change of KO1 by crossing with lupus prone B6.Yaa and New Zealand White (NZW) mice, we established the KO1.Yaa mice,F1 and F2 hybrid of KO1 and NZW mice.Results: The KO1.Yaa mice and (KO1 x NZW)F1 mice did not develop the phenotype of RA, but developed lupus phenotype.In (KO1 x NZW) F2 mice, RA, SLE, and Sjogren syndrome developed independently or overlapped in an individual mouse. We found that the B6-derived locus located in the centromeric region on chromosome 12 was significantly associated with all these disease phenotypes, suggesting that this locus may play a role in common process shared by these diseases.Conclusion: Phenotypic specificity depends on the genetic factors sharing RA, SLE, and Sjogren syndrome.
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| Free Research Field |
膠原病リウマチ学
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