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<biogps><data><item key="platform">6</item><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="id">7563</item><item key="factors"><item><item key="GSM1323884"><item key="TREATMENT">M-CSF</item></item></item><item><item key="GSM1323885"><item key="TREATMENT">M-CSF + dexamethasone</item></item></item><item><item key="GSM1323884"><item key="TREATMENT">M-CSF</item></item></item><item><item key="GSM1323885"><item key="TREATMENT">M-CSF + dexamethasone</item></item></item><item><item key="GSM1323884"><item key="TREATMENT">M-CSF</item></item></item><item><item key="GSM1323885"><item key="TREATMENT">M-CSF + dexamethasone</item></item></item></item><item key="ownerprofile_id">arrayexpress_sid</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-54778</item><item key="summary_wrapped">Glucocorticoids (GC) are used as first line therapies for generalized suppression of inflammation (e.g. allergies or autoimmune...</item><item key="pubmed_id">24990080</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">1</item><item key="sample_count">6</item><item key="tags"><item>bone</item><item>bone marrow</item><item>cell</item><item>colitis</item><item>colon</item><item>cytokine</item><item>line</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">glucocorticoid-induced-gene-regulation-in-murine-b</item><item key="geo_id_plat">E-GEOD-54778_A-AFFY-45</item><item key="name">Glucocorticoid induced gene-regulation in murine bone marrow derived monocytes.</item><item key="created">Nov.12, 2014</item><item key="summary">Glucocorticoids (GC) are used as first line therapies for generalized suppression of inflammation (e.g. allergies or autoimmune diseases), but their long-term use is limited by severe side effects. Our previous work has revealed that GC induced a stable anti-inflammatory phenotype in monocytes, the glucocorticoid-stimulated monocytes (GCsM) that we now exploited for targeted GC-mediated therapeutic effects. We demonstrate that GCsM interact with T-cells in suppressing proliferation as well as cytokine release of CD8+ and especially CD4+ T-cells in vitro, and that they support generation of Foxp3+ cells.  We therefore tested their immunosuppressive potential in CD4+ T-cell-induced colitis in vivo. We found that injection of GCsM into mice with already established severe colitis abolishes the inflammation and results in significant clinical improvement within a few days. T-cells recovered from GCsM-treated mice reveal reduced secretion of pro-inflammatory cytokines IFN-&#61543; or IL-17. Furthermore, accumulation of clusters of Foxp3+ CD4+ T-cells were detectable at local sites of inflammation in their colon.   Thus, GCsM are able to modify T-cell responses in vitro and in vivo and are able to down-regulate and clinically cure an established severe T-cell mediated colitis. Bone marrow derived monocytes where cultured 16 h with media containing M-CSF (control monocytes) or media containing M-CSF and dexamethasone (GCsM). In three independent experiments, total RNA from GCsM and control monocytes was isolated and processed for microarray hybridization.</item><item key="geo_gse_id">E-GEOD-54778</item><item key="species">mouse</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-54778/samples/</item></data></biogps>
