| Project/Area Number |
24700438
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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 |
Laboratory animal science
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
OGAWA Shuuhei 東京理科大学, 生命医科学研究所, 助教 (20385553)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 疾患モデル / 全身性強皮症動物モデル / GVH病 / T細胞 / CD28 / 補助シグナル / 制御性T細胞 / 病態モデル / GVH病動物モデル |
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| Research Abstract |
In patients receiving allogeneic hematopoietic cell transplantation (HCT), chronic graft-versus-host disease (cGVHD) resembles autoimmune diseases such as systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). In this study, we investigated the function of host T cells on symptoms in cGVHD. CD28-deficient mice as hosts showed an SSc-type cGVHD phenotype; in contrast, WT hosts showed an SLE-type cGVHD phenotype. Adoptive cell transfer experiments demonstrated that defects in host CD4+CD25+ Treg, but not in conventional CD4+ T cells were responsible for phenotypic conversion. Furthermore, the defect of host Treg cells altered the cytokine pattern of donor CD4+ T cells might lead to phenotypic change of cGVHD. Thus, host's CD28 signaling, particularly the pathway that drives Treg development, and host Treg cells played a protective role of the development of SSc-type cGVHD.
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