A FUNCTIONAL ROLE FOR INTERLEUKIN (IL)-4-DRIVEN CYCLIC AMP ACCUMULATION IN HUMAN B LYMPHOCYTES
Interleukin-4 (IL-4) regulates the expression of the 55-kDa α-subunit (CD25) of the IL-2 receptor complex in human B lymphocytes. This report suggests that the cAMP/protein kinase A (PKA) component of the IL-4 receptor signalling programme in human tonsillar B cells has a functionally important role...
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| Veröffentlicht in: | Cytokine (Philadelphia, Pa.) Pa.), 2000-06, Vol.12 (6), p.731-736 |
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| container_title | Cytokine (Philadelphia, Pa.) |
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| creator | McKay, Catriona E Hewitt, Ellen L Ozanne, Bradford W Cushley, William |
| description | Interleukin-4 (IL-4) regulates the expression of the 55-kDa α-subunit (CD25) of the IL-2 receptor complex in human B lymphocytes. This report suggests that the cAMP/protein kinase A (PKA) component of the IL-4 receptor signalling programme in human tonsillar B cells has a functionally important role in regulating expression of the CD25 gene by attenuating activity of a protein binding to a potent negative regulatory element (NRE) in the CD25 promoter; this effect can be mimicked by agents that elevate cAMP and blocked by inhibitors of PKA but not protein kinase C (PKC). In a B-cell line that fails to elevate cAMP, attenuate NRE-binding protein (NRE-BP) activity or express CD25 following IL-4 treatment, stimulation of cAMP accumulation by forskolin facilitates IL-4-mediated induction of both the endogenous gene and an exogenous reporter gene under the control of a minimal promoter/enhancer fragment of the CD25 gene. |
| doi_str_mv | 10.1006/cyto.1999.0627 |
| format | Article |
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This report suggests that the cAMP/protein kinase A (PKA) component of the IL-4 receptor signalling programme in human tonsillar B cells has a functionally important role in regulating expression of the CD25 gene by attenuating activity of a protein binding to a potent negative regulatory element (NRE) in the CD25 promoter; this effect can be mimicked by agents that elevate cAMP and blocked by inhibitors of PKA but not protein kinase C (PKC). In a B-cell line that fails to elevate cAMP, attenuate NRE-binding protein (NRE-BP) activity or express CD25 following IL-4 treatment, stimulation of cAMP accumulation by forskolin facilitates IL-4-mediated induction of both the endogenous gene and an exogenous reporter gene under the control of a minimal promoter/enhancer fragment of the CD25 gene.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>10843754</pmid><doi>10.1006/cyto.1999.0627</doi><tpages>6</tpages></addata></record> |
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| ispartof | Cytokine (Philadelphia, Pa.), 2000-06, Vol.12 (6), p.731-736 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | B-Lymphocytes - drug effects B-Lymphocytes - physiology Cells, Cultured Colforsin - pharmacology Cyclic AMP - metabolism Cyclic AMP-Dependent Protein Kinases - metabolism Enzyme Inhibitors - pharmacology Gene Expression Regulation - drug effects Humans IL-4 receptor/CD25 expression/cAMP/human B Lymphocytes Interleukin-4 - pharmacology Isoquinolines - pharmacology Kinetics Palatine Tonsil - immunology Receptors, Interleukin-2 - genetics Receptors, Interleukin-4 - physiology Signal Transduction Sulfonamides |
| title | A FUNCTIONAL ROLE FOR INTERLEUKIN (IL)-4-DRIVEN CYCLIC AMP ACCUMULATION IN HUMAN B LYMPHOCYTES |
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