BMB Reports
- 제30권6호
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- Pages.431-437
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- 1997
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- 1976-670X(eISSN)
Intracellular Signaling Pathways for Type II IgE Receptor (CD23) Induction by Interleukin - 4 and Anti - CD40 Antibody
- Kim, Hyun-Il (Department of Biology, College of Natural Science, Sung Kyun Kwan University) ;
- Park, Hee-Jeoung (Department of Biology, College of Natural Science, Sung Kyun Kwan University) ;
- Lee, Choong-Eun (Department of Biology, College of Natural Science, Sung Kyun Kwan University)
- 투고 : 1997.09.20
- 발행 : 1997.11.30
초록
Since the role of CD40 on the interleukin-4(IL-4) -induced B cell activation has been strongly implicated in the agumentation of IgE production and response, we have investigated the intracelluar signaling pathways utilized by IL-4 and CD40 for type II IgE receptor (CD23) expression. IL-4 and anti-CD40 antibody treatment of human B cells, independently caused a rapid induction of CD23 gene activation within 2 h. There was a noticeable synergism between the action of the two agents inducing CD23 expression: the addition of anti-CD40 to the IL-4-treated culture significantly agumented the IL-4-induced CD23 on both mRNA and surface protein levels, and the inclusion of IL-4 in the anti-CD40-treated cells caused a further increase of CD23 expression far above the maximal level induced by anti-CD40. Protein tyrosine kinase (PTK) inhibitors effectively suppressed the both IL-4- and anti -CD40-induced CD23 expression. whereas protein kinase C (PKC) inhibitors had no effects. Electrophoretic mobility shift assays (EMSA) have shown that IL-4 and anti-CD40 induce the activation of NF-IL-4 and