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Pharmacological modulation of dendritic cell function by anti-inflammatory dexamethasone but not by GSH depletion | ||
| Mustansiriya Medical Journal | ||
| Article 1, Volume 15, Issue 2, 2016, Pages 60-68 | ||
| Author | ||
| Bassim I Mohammad | ||
| Abstract | ||
| The principal function of dendritic cells (DCs) is to acquire antigens from the environment and present them to naïve T-cells to initiate an immune response. DCs also provide potent co-stimulatory signals to T-cells through expression of co-stimulatory receptors such as CD40 and CD86. Anti-inflammatory and other drugs that deplete intracellular glutathione (GSH) can affect the immune response. However, it is unclear whether these drugs can modulate DC function. In this study, we evaluated the effects of the anti-inflammatory drug dexamethasone and the GSH lowering compound as buthionine sulfoximine (BSO) on DC function. Mouse bone marrow derived dendritic cells (BMDCs) were generated and treated with dexamethasone or BSO. Expression of the co-stimulatory molecules MHCII, CD86 and CD40 was quantified by flow cytometry. Endocytic and phagocytic capacity of DCs was measured by dextran uptake and necrotic cell phagocytosis respectively. We found that dexamethasone reduces the expression of co-stimulatory molecules both in immature and mature DCs. Dexamethasone had a marginal increase in the endocytic capacity of iDCs but caused a decrease in phagocytic function. Reducing GSH levels did not affect co-stimulatory molecules expression, endocytic and phagocytic capacity of iDCs. We conclude that anti-inflammatory corticosteroids could modulate the immune response by down regulating DC co-stimulatory molecule and by inhibition of phagocytosis. Further work is needed to examine the ability of dexamethasone treated DCs to stimulate T-cell activation. These findings have | ||
| Keywords | ||
| Dexamethasone; GSH; stimulation; Phagocytosis; endocytosis | ||
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