| Project/Area Number |
13670899
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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 |
Dermatology
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| Research Institution | Kyorin University School of Medicine |
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Principal Investigator |
HAYAKAWA Jun Kyorin University School of Medicine, Department of Dermatology, Instructor, 医学部, 助手 (30255393)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUKAWA Yoshiko Kyorin University School of Medicine, Department of Dermatology, Instructor, 医学部, 助手 (50301479)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | γδ T cell / Th1 / Th2 cytokine / atopic dermatitis / animal model / hapten / neutrophils / 即時型反応 / lgE / γσ^+T細胞 / 接触皮膚炎 / タイプ1反応 / タイプ2反応 / LPR / DETC |
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| Research Abstract |
In this study, we investigated the role of γδ T cells in the regulation of the balance of Th1 and Th2 responses, using a mouse model for atopic dermatitis (AD): we previously demonstrated that chromic epicutaneous exposure to a hapten induces a shift in the pattern, of antigen-induced cytokine expression toward the induction of Th2 cytokines in a site-restricted fashion and that inflammatory responses. in the chronic lesions share many of the histopathological, immunological and clinical features with those of human AD. We asked whether the shift to the Th2 response could be also observed in γδ T cell-deficient mice repeatedly exposed to the hapten. Our results show that depletion of γδ T cells in the epidermis resulted in prolonged and exacerbated inflammation of the skin sites after a few exposure to the hapten and the shift to Th-2 dominated immune responses after repeated application was accelerated. The skin lesions in γδ T cell-depleted mice after repeated exposure to the hapten were rich in neutrophils and there was extensive epidermal damage. Thus, γδ T cell depleted mice are highly susceptible to the induction of Th-2 dominated immune responses associated, with neutrophil infiltration. This phenotype was reduced by adoptiye transfer of γδ T cells to γδ T cell-depleted mice. These results indicate that γδ T cells, exert regulatory functions most likely through their capacity to promptly release cytokines and that absence of γδ T cells favors the development of immune responses toward a Th2 responses ; presence of γδ T cells resident in the epidermis provides protection against excessive inflammatory damage.
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