1997 Fiscal Year Final Research Report Summary
Research for the immunological manipulation of antibody formation in allergic disorders
| Project/Area Number |
08457223
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Fukui Medical University (1997)
Kyoto University (1996) |
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Principal Investigator |
MAYUMI Mitsufumi Fukui Medical University School of Medicine, Department of Pediatrics, Professor, 医学部, 教授 (70135581)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Adhesion / Allergy / Apoptosis / CD40 / Differentiation / Fas / Helper T cell |
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| Research Abstract |
Cellular and molecular basis for activation and differentiation of B-and T-cells was examined.
In B cells, antigen-specific signals through surface Ig cause B cell apoptosis. The antigen-induced B cell death is inhibited by signals through CD40, and LFA-1/ICAM-1-dependent cell a dhesion induced by signals through CD40 plays an important role in the inhibition of B cell death.
IL-7 receptor alpha chain gene was transfected in EBV-transformed B cells established from two X-linked severe combined immunodeficiency patients. The IL-7 receptor expressing B cells which lack common gamma chains are useful to examine the signal transduction mechanisms of IL-7 receptor in human B cells.
In T cells, antigen-specific signals through T cell receptors cause apoptosis of activated human mature T cells in a Fas/Fas ligand-dependent manner. The T cell death is inhibited by adhesion of T cells with monocytes which does not reduce Fas expression on T cells but inhibits death signal transduction through Fas.
Prostaglandin E2 and IL-4 show an additive effect on selective differentiation of Th2 cells from human cord blood naive helper T cells. IL-7 induces proliferation and activation of cord blood naive helper T cells without stimulation through T cell receptor. The activated helper T cells can produce variable cytokines including IL-4 and gamma-interferon by stimulation with calcium ionophore and PMA.
These results are important to understand the basis for immunological manipulation of IgE formation in allergic patients.
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