2004 Fiscal Year Final Research Report Summary
Two faces of IgE-mediated allergic reactions.
| Project/Area Number |
15591048
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YAMAGUCHI Masao The University of Tokyo, Faculty of Medicine, Assistant, 医学部附属病院, 助手 (10302704)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAI Koichi Juntendo University, Faculty of Medicine, Visiting Associate Professor, 大学院・医学系研究科, 客員助教授 (10156630)
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| Project Period (FY) |
2003 – 2004
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| Keywords | allergy / basophils / IgE |
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| Research Abstract |
We tested the possibility that IgE crosslinking stimulation may act on FcεRI-bearing cells via paradoxical effects : namely activation versus inhibition of activation. Using human basophils, we found that IgE-mediated weak stimulation consistently induces profound inhibition of basophil releasability against subsequent, IgE-mediated strong stimulation. Intracellular amount of tyrosine kinases, Lyn, Syk, and Btk were semiquantified using intracellular FACS analysis ; however, the amount of these kinases, as shown by their fluorescence intensity, did not change in the treated cells, compared to untreated cells. Interestingly, the delicate balance of IgE and anti-IgE was important in regulating the fate of cellular releasability ; when anti-IgE antibody is too excess, the basophils are immediately activated, but when IgE and anti-IgE antibody are balanced, the cells lose their releasability without releasing their granule contents (demonstrating desensitization).
These results imply that IgE-mediated effects on FcεRI-bearing cells are not just cellular stimulation ; IgE can mediate complicated effects on the following IgE-mediated cellular response. The balance between IgE and antigen may be critical in regulating the extent of cellular activation. These results may be important in understanding the pathogenesis of complicated alteration of allergic inflammation under local, continuous antigen exposure.
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