1. Author's Information
    H.A. El-Bahrawy
    Department of Biochemistry, Faculty of Pharmacy, Tanta University, Egypt

    G.M. Al-Ashmawy
    Department of Biochemistry, Faculty of Pharmacy, Tanta University, Egypt

    M.L. Salem
    Department of Immunology, Faculty of Science, Tanta University, Egypt

    N.E. El-Ashmawy
    Department of Biochemistry, Faculty of Pharmacy, Tanta University, Egypt

    E.A. El-Zamarany
    Department of Clinical Pathology, Faculty of Medicine, Tanta University, Egypt

  2. Abstract
    Background: Glucocorticoids are known to suppress the immune response and are widely used as immunosuppressive agents in the treatment of many autoimmune and allergic diseases. Aim: This study investigated the effect of the steroid dexamethasone (DEX) on maturation and differentiation of DCs derived from monocytes. In addition, an in vivo experiment was conducted to investigate whether treatment of mice with DEX has immunomodulatory effect on murine splenic DCs. Methods: In vitro experiment: Immature DCs were generated by incubating peripheral blood monocytes with cytokine cocktail (GM-CSF+IL-4) for 9 days. Phenotypic analysis of the DCs’ specific cell marker CD83 was performed by flow cytometry. In vivo experiment: Mice were randomly divided into 5 groups according to the dose of i.p., injection of DEX and duration of treatment. The murine splenic DCs were isolated and phenotyped for CD83 and CD11c by flow cytometry. Results: Addition of 1 μM DEX to the culture on day 7 or 8 resulted in a significant increase in the CD83 expression. The in vivo experiment showed that i.p. injection of DEX significantly increased the expression of CD83 on splenic DCs. Mice groups treated with a single dose of 20 mg kg–1 DEX showed a significant decrease of percentage of CD11c+CD83+ splenic DCs. Conclusion: DEX induced the DCs to be more tolerogenic both in vitro and in vivo. It could be suggested that DEX can trigger immunosuppressive effect via modulating the expression of the cell surface markers of DCs.
    Keywords

    ADLID: 40217-v1
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