Autor: |
Baldeón ME; Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA., Chun T, Gaskins HR |
Jazyk: |
angličtina |
Zdroj: |
The American journal of physiology [Am J Physiol] 1998 Jul; Vol. 275 (1), pp. C25-32. |
DOI: |
10.1152/ajpcell.1998.275.1.C25 |
Abstrakt: |
To better clarify individual roles of interferon (IFN)-alpha and IFN-gamma in beta-cell pathology during the onset of type 1 diabetes mellitus, we compared the effects of these cytokines on insulin production and major histocompatibility complex (MHC) gene expression in pancreatic beta-cell lines. IFN-gamma but not IFN-alpha decreased secreted and intracellular insulin concentrations in betaTC6-F7 and betaTC3 cells. Likewise, IFN-gamma but not IFN-alpha treatment of beta-cells upregulated mRNA expression of MHC class IA antigen-processing genes and surface expression of class IA molecules. Alternatively, class IA MHC expression was upregulated by IFN-gamma and IFN-alpha in the P388D1 macrophage cell line. The observation of constitutive Ifn-alpha6 mRNA expression by a differentiated beta-cell line substantiates previous indications that local expression of IFN-alpha in islets may trigger insulitis. Evidence that IFN-gamma, a product of infiltrating leukocytes, directly decreases beta-cell glucose sensitivity and increases MHC class IA cell surface expression supports the postulate that IFN-gamma magnifies the insulitic process. |
Databáze: |
MEDLINE |
Externí odkaz: |
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