1996 Fiscal Year Final Research Report Summary
REGULATION OF INFLAMMATORY AND ALLERGY RESPONSES BY ANTI-LFA-1 MONOCLONAL ANTIBODY
| Project/Area Number |
07670382
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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 |
Immunology
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| Research Institution | TOKAI UNIVERSITY |
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Principal Investigator |
NISHIMURA Takashi TOKAI UNIVERSITY,SCHOOL OF MEDICINE,ASSOCIATE PROFESSOR, 医学部, 助教授 (30143001)
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| Co-Investigator(Kenkyū-buntansha) |
HABU Sonoko TOKAI UNIVERSITY,SCHOOL OF MEDICINE,PROFESSOR, 医学部, 教授 (30051618)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Th1-Th2 balance / liver injury / allergy / LFA-1 / T cells / IL-12 / IgE / Cytokine |
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| Research Abstract |
In this project, we demonstrated that mouse liver injury model induced by propionibacterium acnes (P.acnes) plus LPS is T cell-dependent one judging from the experiment using T cell deficient nude mice. Because the liver injury was completely blocked by anti-LFA-1 mAb, LFA1-ICAM-1 interaction is essential for the activation and migration of effector cells to liver. It was also demonstrated that Th1-activating cytokine, IFN-gamma and IL-12 are key cytokines in this liver injury model. C57BL/6 mice, which are prone to show Th1 immunity, are sensitive to P.acnes plus LPS-induced liver injury, while BALB/c showing Th2 immunity are resistant to this. Therefore, genetically-controlled Th1/Th2 balance appeared to be important factor the induction of liver injury.
The important role of LFA-1 molecule in allergy is also demonstrated from the evidence that anti-LFA-1 mAb administration inhibited IgE production in vivo for long-term.
Thus, the important role of LFA-1 molecule and Th1-Th2 balances in the regulation of liver inflammatory responses and allergy was clearly demonstrated by this project.
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