A Defense Mechanism from Superantigens in Chronic Inflammatory Bowel Disease.
Project/Area Number |
06670811
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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 |
Pediatrics
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Research Institution | KAGOSHIMA UNIVERSITY |
Principal Investigator |
TAKEI Shuji (1996) University Hospital Kagoshima University, Assistant Professor, 医学部附属病院, 講師 (60175437)
今中 啓之 (1994-1995) 鹿児島大学, 医学部・付属病院, 助手 (80223329)
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Co-Investigator(Kenkyū-buntansha) |
奥 章三 鹿児島大学, 医学部・付属病院, 助手 (80224145)
武井 修治 鹿児島大学, 医学部・付属病院, 講師 (60175437)
|
Project Period (FY) |
1994 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
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Keywords | Superantigen / Chronic inflammatory bowel disease / Staphylococcus aureus / Group A streptococi / Gammaglobulin / Epitope / SEB / 生体防御 / スーパーアンチゲン / 溶連菌 / ELISA |
Research Abstract |
A humoral defense mechanism for superantigens (SA) was investigated in both healthy children and patients with chronic inflammatory bowel diseases (CIBD) by using staphylococcal enterotoxin B (SEB), and streptococcal pyrogenic exotoxin (SPE) A (SPE-A) and C (SPE-C). Specific antibodies (Abs) to SEB, SPE-A,and SPE-C were found in healthy children and the positivity of Abs to each SA increased with age. The age at which more than 50% of children exhibited Abs to SA was 1 year for SEB, 6year for SPE-C and 11 year for SPE-A.Sera from these children were inhibitory to T cell proliferation elicited by SA in proportion to the concentration of lgG Ab to each SA.Sera supplemented with lgG Abs to SA by gamma-globulin therapy became inhibitory to T cell proliferation by SA.The B cell epitope mapping examination revealed that dominant epitope was estimated at C region aa 225-234 of recombinant SEB. Patients with CIBD were found to have those specific Abs to SAs which were inhibitory to T cell activation elicited by each SA.Anti-SEB Ab titer was higher in CIBD patients compared with healthy children. T cells from CIBD patients respond normally to SAs, though T cells from some patients with Crohn disease were poorly proliferated by SPE-C stimulation. We conclude that the presence of Ab to SA is one of the humoral defense mechanism for vigorous T cell activation by SA.Further investigation should be developed to examine the the humoral defense system for SA in children not only with CIBD but also with inflammatory diseases such as collagen diseases and Kawasaki disease.
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Report
(4 results)
Research Products
(18 results)