2014 Fiscal Year Final Research Report
Molecular mechanism and regulation of Sjogrens syndrome
Project/Area Number |
24591439
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
膠原病・アレルギー・感染症内科学
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Research Institution | University of Tsukuba |
Principal Investigator |
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Keywords | 自己抗原 / 自己反応性T細胞 / 自己免疫性唾液腺炎 / ムスカリン作動性アセチルコリン受容体 / T細胞エピトープ / IFN-γ / IL-17 / RORγt |
Outline of Final Research Achievements |
To clarify the role of M3R immune response in the generation of Sjogren’s syndrome (SS), we established M3R induced sialadenitis (MIS) mouse model and examined whether M3R reactive T cells trigger the autoimmune sialadenitis or not. In the present study, we obtained evidence that M3R reactive Th1 and Th17 cells were associated with the generation of MIS, the major T cell epitopes of M3R were N1 and the first extra-cellular domain, and one of analogue ligand peptide (APL) coding N1 region could inhibit the induction of sialadenitis significantly. These observations should shed light on the antigen-specific therapy in SS near future.
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Free Research Field |
臨床免疫学
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