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KMID : 0350519930460020635
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Journal of Catholic Medical College
1993 Volume.46 No. 2 p.635 ~ p.646
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The Effect of Interleukin-4, Interferon-γand Hydrocortisone on the Expression of FcεR II and soluble FcεR II Production on B Cells in Allergic Individuals
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Abstract
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Two types of receptors on the Fc portion of human IgE(FcεR) differ in their affinity for IgE as well as in their cellular distribution and function.
Type 1 FcεR I) show high affinity for IgE and are detectable on mast cells and basophils. The reaction between allergen and IgE bound to FcεR I induces degranulation of basophils and mast cells, with release of chemical mediators responsible
for
the
clinical manifestations of allergy.
Type 2 FcεR (FcεRⅡ) bind IgE with lower affinity and are present on monocytes, macrophages, lymphocytes, platelets and eosinophils. The binding of IgE to FcεRⅡ activates a various effector functions in these cells.
Interleukin-4(IL-4) and interferon-γ(IFN-γ) secreted from the T lymphocytes(cells) have influence on the production of IgE through the expression of FcεRⅡon B cells and it´s cleaving product soluble FcεRⅡ(sFcεRⅡ), therefore they play an
important role as an immunologic factors in allergy.
This study was performed to evaluate the interactions among these lymphokines and hydrocortisone, and also their roles in the expression of FcεRⅡ and the production of sFcεRⅡon B cells.
The expression of FcεRⅡon B cells from normal and allergic individuals were measured by fluorescnet activated cell sorter (FACS) after double staining with anti Leu 16-FITC and anti Leu 20-PE and sFcεRⅡproductions were measured by enzyme
linked
immunosorbent assay(ELISA). In-teractions between IL-4 and IFN-γor hydrocortisone in the expression of FcεRⅡ and the production of sFcεRⅡwere observed.
@ES The results were as follows ;
@EN 1. Positive expression of FcεRⅡ on B cells in the peripheral blood was 28.4±11.7% in normal individuals and 54.7±18.3% in allergic individuals. Positive expression in allergic individuals increased about 2 times compared with that of
normal
individuals.
2. Positive expression of FcεRⅡon cultured B cells without IL-4 in normal and allergic individuals were 5.3±2.4% and 6.8±3.2% respectively. When 2 u/ml of IL-4 was added, positive expression of FcεRⅡbegan to increase gradually in both
groups(10.2±4.5%, 13.9±4.9%). When 20 u/ ml of IL-4 was added, the highest value of positive expression of FcεRⅡwas observed in normal and allergic individuals(62.7±18.5%, 64.4±21.4%, P<0.0001), and retained thereafter. There were no
significant
differences between two groups.
3. When IFN-γε100 u/ml was added to IL-4 20 u/ml, positive expression of FcεRⅡbegan to decrease both in normal and allergic individuals(47.2±15.4, 49.8±13.2%). With 10,000 u/ml of IFN-γ the positive expression of FcεRⅡ decreased
significantly
in normal and allergic individuals(21.7±8.4%, 24.9±10.9%, P<0.0001). Inhibitory effect of IFN-γon IL-4 induced FcεRⅡexpression showed dose-dependent pattern. There were no significant differences between two groups.
4. When 10-E8 M hydrocortisone was added to IL-4 20 u/ml, positive expression of FcεRⅡbegan to decrease in normal and allergic individuals(59.2±28.5%, 61.8±22.4%). When hydrocotisone increased to 10E-7 M, positive expression of FcεⅡRabove
that
concentration. There were no significant differences between two groups.
5. The concentration of sFcεRⅡin cultured B cells supernatant in normal and allergic individuals increased slightly at 20 u/ml of IL-4. The maximum increase of sFcεRⅡwas noted in normal (106.5±32.5 u/ml) and allergic individuals(116.4±31.8
u/ml)
at 100 u/ml of IL-4. IFN 1,000 u/ml or hydrocortisone 10E-6 M was added to IL-4 100 u/ml, the concentration of sFcεRⅡdecreased significantly in normal(69.2±69.2±20.9 u/ml, 53.2±13.2 u/ml) and allergic individuals(68.9±22.5 u/ml, 59.1±17.5
u/ml).
And cultured with IL-4 100 u/ ml and IFN-γ10,000 u/ml or hydrocortisone 10E-4 M, the concentration was significantly decreased in normal (51.7±14.4 u/ ml, 33.8±9.3 u/ml) and allergic individuals(45.8±12.6 u/ml, 32.7±11.0 u/ml). The
antagonistic
effect of IFN-γor hydrocortisone on sFcεRⅡproduction by IL-4 was dose-dependent.
These results suggest that enhaced FcεRⅡexpression on peripheral blood B cells in allergic individuals may be related to the increased level of IL-4 in vivo rather than increased B cell activity to IL-4 in allergic individuals. And IL-4 induced
FcεRⅡexpression and sFcεRⅡproduction were inhibited by IFN-γor hydrocortisone.
In conclusion, the interactions and imbalance of these lymphokines and hormone play an important role in the immuopathogenesis of allergy.
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KEYWORD
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