2004 Fiscal Year Final Research Report Summary
Molecular biological approach to allergy disease medical treatment
| Project/Area Number |
15591065
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Showa University |
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Principal Investigator |
TOBE Takashi Showa Univ., Pharmaceutical Sciences, Professor, 薬学部, 教授 (90102368)
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| Co-Investigator(Kenkyū-buntansha) |
NAKANO Yasuko Showa Univ., Pharmaceutical Sciences, Assistant Professor, 薬学部, 助教授 (20155790)
NEGORO Takaharu Showa Univ., Pharmaceutical Sciences, Assistant Researcher, 薬学部, 助手 (70218270)
NARUSHIMA Michiaki Showa Univ., Medical School, Assistant Professor, 医学部, 助教授 (30255856)
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| Project Period (FY) |
2003 – 2004
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| Keywords | CD25^<high>CD4+Tregs / asthma / Ca^<2+> responses / anergy / CD45RO^+ T細胞 / Ca^<2+>不応答性 / anergy |
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| Research Abstract |
Objective : The aim of this study was to investigate whether the functions of the CD25^<high> CD4+Tregs including regulation of CD25^-T cells activation and the Ca^<2+> response to T cell receptor (TCR) stimulation as a marker of anergy are changed in asthma. Methods: Blood samples were collected from the outpatients of Showa University Fujigaoka Hospital and Showa University. Ca^<2+> response were analyzed with fluoroimaging technique. Proliferation was analyzed by flow cytometry.
Results : The CD25^<high> CD4+ Tregs from non-asthmatics were unresponsive to TCR stimulation, resulting in paucity of proliferation and Ca^<2+> response. However, in contrast to non-asthmatics, the CD25^<high> CD4+ Tregs from asthmatics were responsive to the stimulation, and the Ca^<2+> response pattern could be classified into two groups, Type 1 and Type 2. Type 1 cells exhibited normal Ca^<2+> response in most of cells, and showed enforced proliferation and weaker regulatory functions compared to the normal ones. In contrast, Type 2 cells were responsive but had a slight increase in intra-cellular Ca^<2+>, and partially functioned as regulatory cells.
Conclusion : We identified impaired Ca^<2+> responses in CD25^<high>CD4+ Tregs from non-asthmatics but increasing Ca^<2+> responses in the cells from asthmatics upon TCR engagement. These observations suggested that abnormalities of CD25^<high>CD4+ Tregs in asthmatics are implicated in the chronic inflammation in the airway.
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