1998 Fiscal Year Final Research Report Summary
Role of Valpha24JalphaQ TCR T Cells in the Pathogenesis of Asthma
Project/Area Number |
09670600
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
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Research Institution | Chiba University Scool of Medicine |
Principal Investigator |
IWAMOTO Itsuo Chiba University, Associate Professor, 医学部, 助教授 (10111436)
|
Co-Investigator(Kenkyū-buntansha) |
KURASAWA Kazuhiro Chiba University, Assistant, 医学部, 助手 (30282479)
KURASAWA Kazuhiro Chiba University, Assistant (30282479)
KURASAWA Kazuhiro Chiba University, Assistant (30282479)
KURASAWA Kazuhiro Chiba University, Assistant (30282479)
KURASAWA Kazuhiro Chiba University, Assistant (30282479)
|
Project Period (FY) |
1997 – 1998
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Keywords | Asthma / Valpha24JalphaQ TCR / NK T cells / IFN-gamma / Th2 cells / Th2タイプ免疫応答 |
Research Abstract |
Atopic disorders are caused by disregulated activation of T helper 2 (Th2) cells that produce IL-4 and IL-5, Because the presence of IL-4 potently augments the differentiation of naive T cells into Th2 cells, it is important to seek the cell population which provides IL- 4 for naive T cells. Recently, a unique subpopulation of T cells, natural killer (NK) T cells, has been shown to produce a large amount of IL-4 upon activation, suggesting their regulatory role in initiation of Th2 cell differentiation. To determine whether NK T cells play a role in human Th2 diseases, we analyzed the NK T cells in patients with asthma and atopic dermatitis (AD). We performed a frequency analysis of the invariant Valpha24JalphaQ CD4^-CD8^- T cells, probable human NK T cells, and found that the NK T cells are significantly decreased in patients with asthma and AD.In addition, we found that the majority of human NK T cells from healthy subjects produce IFN-gamma but not IL-4 upon activation. Taken together, these results suggest that the decrease of NK T cells, which produce IFN-y, may be involved in the pathogenesis of atopic diseases, such as asthma and AD.
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