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- Title
IGF-1 Potentiation of IL-4-induced CD23/FcεRII Expression in Human B Cells.
- Authors
Kim, Jeong-Ho; Park, Hyun-Hee; Lee, Choong-Eun
- Abstract
Interleukin-4 (IL-4) is a major cytokine regulating IgE production and IgE response. Neuroendocrine growth pactors, such as growth hormone and insulin-like growth factor 0GF-I), also modulate IgE production by human B cells. "We report that in both human primary immune cells and established B cell lines, IGF-I increased expression of the IL-4-induced type II IgE receptor (FcεRll/CD23). This effect was also seen at the mRNA level. IGF-1 increased the activity of signal transducer and activator of transcription 6 (STAT6) in response to IL-4, and activated NF-kB. STAT6 and NF-kB are major transcription factors controlling CD23 expression. The tyrosine kinase inhibitor, tyrphostin, abolished both IL-4- and IL-4 plus IGF-Imediated induction of STAT6 and tile subsequent CD23 expression. In contrast, pyrrolidine dithiocarbamate (PDTC), an NF-kB inhibitor, only suppressed the enhancing effect of IGF-I on IL-4-induced CD23 expression. Our data suggest that IGF-I modulates CD23 gene expression by affecting the STAT6 and NFkB pathways. Regulation of CD23 by IGF-I may have an important implication for the immunomodulatory potential of IGF-1, and may provide a new therapeutic target for allergy and other hypersensitivity reactions involving an excessive IgE response.
- Subjects
INTERLEUKINS; CYTOKINES; GROWTH factors; CELLULAR immunity; PROTEIN-tyrosine kinases
- Publication
Molecules & Cells (Springer Nature), 2003, Vol 15, Issue 3, p307
- ISSN
1016-8478
- Publication type
Article
- DOI
10.1016/s1016-8478(23)13742-3