| Literature DB >> 19776014 |
Michael W Harr1, Yiping Rong, Martin D Bootman, H Llewelyn Roderick, Clark W Distelhorst.
Abstract
Glucocorticoids are potent immunosuppressive agents that block upstream signaling events required for T cell receptor (TCR) activation. However, the mechanism by which glucocorticoids inhibit downstream responses, such as inositol 1,4,5-trisphosphate (IP(3))-induced calcium signals, is not completely understood. Here we demonstrate that low concentrations of dexamethasone rapidly convert transient calcium elevations to oscillations after strong TCR stimulation. Dexamethasone converted the pattern of calcium signaling by inhibiting the Src family kinase Lck, which was shown to interact with and positively regulate Type I IP(3) receptor. In addition, low concentrations of dexamethasone were sufficient to inhibit calcium oscillations and interleukin-2 mRNA after weak TCR stimulation. Together, these findings indicate that by inhibiting Lck and subsequently down-regulating IP(3) receptors, glucocorticoids suppress immune responses by weakening the strength of the TCR signal.Entities:
Mesh:
Substances:
Year: 2009 PMID: 19776014 PMCID: PMC2797257 DOI: 10.1074/jbc.M109.005579
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157