Thu, 21 Aug 2008 15:11:27 BST CiteULike: AlfonsoVicenteSuarez's il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/tag/il-10-general CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1452726 <i></i> A Prominent Role for Sp1 During Lipopolysaccharide- Mediated Induction of the IL-10 Promoter in Macrophages -- Brightbill et al. 164 (4): 1940 -- The Journal of Immunology 2007-07-12T16:25:53-00:00 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1452697 <i></i> Functional Analysis of -571 IL-10 Promoter Polymorphism Reveals a Repressor Element Controlled by Sp1 -- Steinke et al. 173 (5): 3215 -- The Journal of Immunology 2007-07-12T16:02:19-00:00 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1452644 <i>J Immunol, Vol. 165, No. 1. (1 July 2000), pp. 286-291.</i><br /><br />IL-10 is an 18-kDa cytokine with a key role in homeostatic control of inflammatory and immune responses. We have investigated how transcription of the IL-10 gene is regulated, so as to be able to understand the circumstances of IL-10 expression in both health and disease. In the mouse, IL-10 gene expression is regulated by a TATA-type promoter with a critical cis-acting element containing GGA repeats located at -89 to -77. Its complementary sequence is similar to the cis-acting elements (TCC repeats) in the promoters of genes encoding epidermal growth factor receptor and CD58. All these elements comprise a common CCTCCT sequence with less conserved C + T-rich sequences. Eliminating this CCTCCT sequence results in a marked reduction in promoter activity, suggesting a necessary role in IL-10 gene expression. Despite its dissimilarity to the G + C-rich Sp1 consensus sequence (GC box), Sp1 and Sp3 transcription factors could be shown to bind to this motif. The requirement for Sp1 and Sp3 in transcription of IL-10 was confirmed using Drosophila SL2 cells, which lack endogenous Sp factors. These results suggest that the transcription of IL-10 is positively regulated by both Sp1 and Sp3. IL-10 Gene Expression Is Controlled by the Transcription Factors Sp1 and Sp3 Masahide Tone Mark Powell Yukiko Tone Sara Thompson Herman Waldmann J Immunol, Vol. 165, No. 1. (1 July 2000), pp. 286-291. 2007-07-12T15:33:49-00:00 2000 J Immunol 165 1 286 291 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1452631 <i></i> Posttranscriptional Regulation of IL-10 Gene Expression Through Sequences in the 3'-Untranslated Region -- Powell et al. 165 (1): 292 -- The Journal of Immunology 2007-07-12T15:27:32-00:00 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1392505 <i>J Immunol, Vol. 175, No. 2. (15 July 2005), pp. 1041-1046.</i><br /><br />The molecular mechanisms that regulate expression of the immunosuppressive cytokine IL-10 remain poorly understood. In this study, by measuring sensitivity to DNase I digestion, we show that production of IL-10 by primary mouse bone marrow-derived macrophages stimulated through pattern recognition receptors was associated with chromatin remodeling of the IL-10 locus. We also demonstrate that the IL-10 locus is remodeled in primary Th2 cells and IL-10-producing regulatory T cells that have been differentiated in vitro. Strikingly, a novel DNase I-hypersensitive site (HSS-4.5) was identified in stimulated macrophages, but not in T cells. We show that hyperacetylated histones were recruited to this site in stimulated macrophages. Furthermore, HSS-4.5 is highly conserved and contains a putative NF-kappaB binding site. In support of a function for this site, NF-kappaB p65/RelA was recruited to HSS-4.5 in vivo and its activation was required for optimal IL-10 gene expression in LPS-stimulated macrophages. Identification of a Macrophage-Specific Chromatin Signature in the IL-10 Locus Margarida Saraivaparagraph Jillian Christensen Alla Tsytsykova Anne Goldfeld Steven Ley Dimitris Kioussis Anne O'Garra J Immunol, Vol. 175, No. 2. (15 July 2005), pp. 1041-1046. 2007-06-15T17:46:35-00:00 2005 J Immunol 175 2 1041 1046 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1392189 <i>Current Opinion in Pharmacology, Vol. 6, No. 4. (August 2006), pp. 379-386.</i><br /><br />Interleukin (IL)-10 performs an irreplaceable role in negatively regulating inflammation, primarily through a mechanism that selectively blocks the expression of pro-inflammatory genes encoding cytokines, chemokines, cell-surface molecules and other molecules involved in the propagation of inflammation. Not surprisingly, IL-10 has attracted interest as a tool to regulate inflammatory diseases. The clinical use of IL-10 as an anti-inflammatory agent has, however, not met expectations. Nevertheless, the signaling pathway used by the IL-10 receptor to generate the anti-inflammatory response is only beginning to be understood and could be a way to regulate inflammation by pharmacological agents. Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response Peter Murray Current Opinion in Pharmacology, Vol. 6, No. 4. (August 2006), pp. 379-386. 2007-06-15T15:42:08-00:00 2006 Current Opinion in Pharmacology 6 4 379 386 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1392182 <i>PNAS, Vol. 102, No. 24. (14 June 2005), pp. 8686-8691.</i><br /><br />The antiinflammatory cytokine IL-10 inhibits the production of multiple, diverse inflammatory mediators from activated macrophages and dendritic cells, a process requiring STAT3 activation. However, the mechanisms involved in the broad inhibitory effects of IL-10 are controversial. I eliminated the contribution of the major confounding variable to understanding the antiinflammatory response, the 3' UTR region of inflammatory mediator genes, through knock-in mutation and analysis of the effects of IL-10 on transcription rate of inflammatory genes. IL-10 activates STAT3 to act indirectly by selectively inhibiting gene transcription independent of general effects on NF-kappaB or posttranscriptional mRNA processing through a process that reduces the overall transcriptional rate of specific genes. 10.1073/pnas.0500419102 The primary mechanism of the IL-10-regulated antiinflammatory response is to selectively inhibit transcription Peter Murray doi:10.1073/pnas.0500419102 PNAS, Vol. 102, No. 24. (14 June 2005), pp. 8686-8691. 2007-06-15T15:38:44-00:00 2005 PNAS 102 24 8686 8691 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1390596 <i></i> INTERLEUKIN-10 AND THE INTERLEUKIN-10 RECEPTOR - Annual Review of Immunology, 19(1):683 - Abstract 2007-06-14T19:57:21-00:00 il-10-general http://www.citeulike.org/user/AlfonsoVicenteSuarez/article/1390588 <i></i> Interleukin-10 and Related Cytokines and Receptors - Annual Review of Immunology, 22(1):929 - Abstract 2007-06-14T19:51:51-00:00 il-10-general