2000 Fiscal Year Final Research Report Summary
Study on the role of dendritic cells in the atopic dermatitis
| Project/Area Number |
11670829
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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 | Osaka University |
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Principal Investigator |
ASADA Hideo Osaka Univ. Grad. School of Med., Lecturer, 医学系研究科, 講師 (60252681)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIKAWA Kunihiko Osaka Univ. Grad. School of Med., Professor, 医学系研究科, 教授 (20110851)
ITAMI Satoshi Osaka Univ. Grad. School of Med., Associate Professor, 医学系研究科, 助教授 (30136791)
SANO Shigetoshi Osaka Univ. Grad. School of Med., Lecturer, 医学系研究科, 講師 (80273621)
TAMURA Manabu Osaka Univ. Grad. School of Med., Associate Professor, 医学系研究科, 助教授 (50273644)
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| Project Period (FY) |
1999 – 2000
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| Keywords | atopic dermatitis / T cell / dendritic cell / cytokine / apoptosis / superantigen / staphylococus aureus / neutralizing antibody |
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| Research Abstract |
It is known that atopic dermatitis (AD) is a Th2 dominant inflammatory skin disease, however, the mechanism of such Th1/Th2 unbalance is unknown. We hypothesized that dendritic cells, professional antigen presenting cells, have an important role to determine Th1/Th2 balance in this disease. We planed to study the role of dendritic cells on Th1/Th2 unbalance in AD.At first, to investigate the immunological status of T cells in AD patients, we assessed the proliferative response of peripheral blood mononuclear cells to staphylococcal enterotoxin B (SEB), one of the superantigens from S.aureus, which have a role in aggravation of AD.Our studies demonstrated that T cells from the patients with severe AD were prone to undergo apoptosis following SEB stimulation, and that not only Th1 but also Th2 activity was suppressed. Dendritic cells were suggested to induce T cell apoptosis. In contrast to this in vitro phenomenon, we observed few apoptotic T cells at the AD lesion with staphylococcal infection. To clarify this discrepancy, we hypothesized that anti-apoptotic activity was present in the serum of the patient. We examined whether or not sera of AD patients had any influence on T-cell response to SEB.We found that sera from severe AD patients had high titers of anti-SEB neutralizing antibody and markedly suppressed T cell proliferative response to SEB.Our findings suggest that anti-SEB neutralizing antibody may rescue T cells from apoptosis and paradoxically down-regulate inflammatory responses induced by SEB in the patients.
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Research Products
(2 results)
