2017 Fiscal Year Final Research Report
Analysis of CD8+CD26-positive/negative T cell subsets for the development of an innovative therapy and elucidating the pathophysiology of refractory autoimmune diseases
| Project/Area Number |
26860760
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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 |
Collagenous pathology/Allergology
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| Research Institution | Juntendo University |
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Principal Investigator |
Hatano Ryo 順天堂大学, 医学(系)研究科(研究院), 特任研究員 (30638789)
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| Research Collaborator |
ISHII Tomonori
SEKIGAWA Iwao
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | CD26/DPPIV / T細胞 / SLE / 自己免疫疾患 / 細胞傷害性T細胞 / 共刺激分子 / ヒト免疫 |
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| Outline of Final Research Achievements |
CD26 is a T cell costimulatory molecule, and CD26+ T cells have been suggested to be involved in the pathophysiology of diverse autoimmune diseases. Since the role of CD26 in the pathophysiology of SLE still remains to be elucidated, our objective is to characterize the CD26-positive or negative T cell subsets in SLE patients. Human CD4+ or CD8+ T cells were purified from PBMCs of SLE patients or healthy adult volunteers, and we examined the phenotypes of CD26-positive or negative subsets. In addition to CD8+CD26nega T cells, CD4+CD26nega T cells were also markedly increased in SLE patients, and these cells exhibited CD28negaCD57+PerforinhiGranzyme Bhi cytotoxic potential. It takes more than 24 months for the patients with a large number of these subsets to reduce the daily dose of prednisolone to less than 10 mg after the initial treatment, strongly suggesting that CD26nega cytotoxic T cells are involved in the pathophysiology of steroid-resistant SLE.
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| Free Research Field |
免疫学
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