1991 Fiscal Year Final Research Report Summary
Analysis of T cell activation by bacterial extoxins bearing MHC class II-binding activity
| Project/Area Number |
02807047
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
細菌学
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| Research Institution | Tokyo Women's Medical College |
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Principal Investigator |
UCHIYAMA Takehiko Tokyo Women's Medical College, School of Medicine, Professor, 医学部, 教授 (00050550)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Hidehito Tokyo Women's Medical College, School of Medicine, Research Associate, 医学部, 助手
YAN Xiao-Jie Tokyo Women's Medical College, School of Medicine, Research Associate, 医学部, 助手 (80195627)
YAGI Junji Tokyo Women's Medical College, School of Medicine, Assistant Professor, 医学部, 講師 (70182300)
IMANISHI Ken'ichi Tokyo Women's Medical College, School of Medicine, Assistant Professor, 医学部, 講師 (20132920)
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| Project Period (FY) |
1990 – 1991
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| Keywords | HUVEC / IFN-r / HLA class II / bacterial exotoxins / TSST-1 / SEs / HUVEC / ILー2 |
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| Research Abstract |
Human umbilical vascular endothelial cells (HUVEC) stimulated with recombinant human IFN-r were inveatigated for expression of HLA class II molecules, toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A(SEA)-binding activity and accessory cell (AC) activity in T cell activation by TSST-1, SEA and related exotoxins. HUVEC stimulated with recombinant human IFN-r ranging from 10 to 3000 U/ml for 72 h express HLA class II molecules. Intensity of the expression was dependent on the concentration of IFN-r. HUVEC stimulated with 1000 U/ml of IFN-r for 72 h exhibited ^<125>I-TSST-1 and SEA-binding that was blocked by the unlabeled coresponding toxins and mAb to DR/DP. The activity was not blocked by paraformaldehyde fixation. The IFN-r-stimulated HUVEC exhibited AC activity in IL-2 production in human peripheral T cells stimulated with the several bacterial exotoxins. The activity was blocked by mAb to DR/DP. In view of the facts that TSST-1 and SEs bind directly to HLA class II molecules and activate human T cells in association with HLA class II molecules on AC, it is likely that the acquisition of the above activities in the toxin-induced T cell activation is mediated by the expression of HLA class II molecules. It seems likely that vascular endothelial cells play an important role in the development of pathological changes in patients suffering an acute and systemic illness TSS.
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