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| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Vassiliadis, S. | en |
| dc.contributor.author | Papadopoulos, G. K. | en |
| dc.date.accessioned | 2015-11-24T19:12:12Z | - |
| dc.date.available | 2015-11-24T19:12:12Z | - |
| dc.identifier.issn | 0962-9351 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/21035 | - |
| dc.rights | Default Licence | - |
| dc.title | IL-6-mediated MHC class II induction on RIN-5AH insulinoma cells by IFN-gamma occurs via the G-protein pathway | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.primary | 10.1155/S0962935195000615 | - |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/18475668 | - |
| heal.identifier.secondary | http://downloads.hindawi.com/journals/mi/1995/139469.pdf | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.publicationDate | 1995 | - |
| heal.abstract | Major histocompatibility complex (MHC) class II antigen expression has been implicated in the pathogenesis of autoimmune type 1 diabetes. In this study we examined the role of various cytoldnes that may induce MHC class II surface antigen expression, using the rat insulinoma line RIN-5AH as a pertinent model system. As in another study, the ability of IFN-gamma to amplify MHC class II antigen expression 4-fold is demonstrated. At the same time we noted a 5-fold increase of these histocompatibility antigens by IL-6. Signal transduction analysis reveals that IL-6-induced MHC class II expression is specifically mediated by the G-protein system (activation of p21(ras) by IL-6) since mevalonic acid lactone (a Gprotein inhibitor) abolishes the action of IL-6. In contrast, IFN-gamma, which does not activate p21(ras), is not inhibited by protein kinase C (PKC) inhibitors but by those of the G-protein pathway. This finding raises the possibility that IFN-gamma induces RIN cells to secrete IL-6 (as shown previously, as well as in this paper) which, in turn, increases class II antigen expression via the G-protein pathway. This action may be unique to IL-6 or in synergy with IFN-gamma. Other cytokines such as IL-1alpha and beta, and TNF-alpha induce a smaller increase in MHC class II antigens on RIN cells, and appear to activate both the G-protein and the PKC signal transduction pathways to varying degrees. Therefore, injury of pancreatic beta-cells and possible induction of autoimmune type 1 diabetes via various cytokines may be caused by IL-6 or IFN-gamma, or by their ability to induce MHC class II antigen upregulation. | en |
| heal.journalName | Mediators Inflamm | en |
| heal.journalType | peer-reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ | |
Files in This Item:
| File | Description | Size | Format | |
|---|---|---|---|---|
| Vassiliadis-1995-IL-6-mediated MHC cl.pdf | 1.17 MB | Adobe PDF | View/Open |
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