| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1988: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1987: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
Regulation of the low affinity LgE receptor (Fc R2/CD23) expression on peripheral mononuclear cells and a human monocytic leukemia cell line U937 was examined. Surface Fc R2(+) cells among human peripheral mononuclear cells were B lymphocytes. T lympho-cytes, when stimulated with mitogens such as PHA, Con A and LPF, secreted factor(s) which induced Fc R2 expression on B lymphocytes. Dexamethasone suppressed the Fc R2 expression. PMA, interferon- (IFN- ), IFN- and 2', 5'-oligoadenylates (2,5-A) increased Fc R2 expression on U937 cells and dexamethasone suppressed it. 2,5-A was suggested to be a mediator of the effect of IFN- but not that of IFN- . The enhancing activity of PMA but not that of IFN- was inhibited by a protein kinase C inhibitor. PMA and IFN- increased the Fc R2 mRNA level in U937 cells but IFN- and 2,5-A did not increase it. Dexamethasone decreased the Fc R2 mRNA expression.
The numbers of Fc R2(+) cells among peripheral blood mononuclear cells and the serum soluble Fc R2 (LgE-binding factor) levels of atopic children younger than 3 years of age were significantly higher than those of non-atopic age-matched control. Such difference was not seen in the older children. The serum LgE levels of atopic children rapidly increased and reached at a plateau around at 3 years of age. The results suggest a close relationship between the activation mechanisms of LgE synthesis and those of Fc R2 expression.
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