Dexamethasone inhibits IFNγ-induced MHC class II expression of intestinal epithelial cells independently of the TGF-β1 regulatory pathway

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In the presence of inflammation, an increased expression of enterocyte MHC class II is observed, leading to altered mucosal antigen handling. Corticosteroids are potent anti-inflammatory drugs, widely used in treating inflammatory bowel disorders. However, their diverse mechanisms of action are only partially understood.


To evaluate effect and mechanisms of corticosteroids on intestinal crypt epithelial cell MHC class II.


The effect of dexamethasone treatment on cytokine-induced MHC class II expression was measured in IEC-6 cells by immunofluorescence and flow cytometry. To determine the role of the TGF-β1 regulatory pathway in mediating the effects of dexamethasone, neutralizing anti-TGF-β antibodies were used. Additionally, endogenous and dexamethasone-stimulated IEC-6 cell TGF-β1 production was measured by ELISA.


Dexamethasone potently down-regulated IFNγ-induced class II expression on IEC-6 cells, in a dose-dependent manner. TGF-β1 had a similar inhibitory effect on class II expression. However, neutralizing anti-TGF-β antibodies did not alter the effect of dexamethasone. Furthermore, dexamethasone reduced endogenous TGF-β1 synthesis.


Corticosteroids inhibit cytokine-induced MHC class II expression on IEC-6 cells in a TGF-β1 independent way. This effect may markedly alter enterocytic antigen presentation, reducing the aberrant state of activation of mucosal immune cells.

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