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Evaluation of the Immunomodulatory Ef-fect of Curdlan on Maturation and Function of Mouse Spleen-Derived Dendritic Cells

Author(s): Mohammad Hashem Soltani | Tahereh Kalantari | Mohammad Hossein Karimi | Nasrollah Erfani | Eskandar Kamali Sarvestani

Journal: Iranian Journal of Immunology
ISSN 1735-1383

Volume: 9;
Issue: 3;
Start page: 168;
Date: 2012;
Original page

Keywords: Dendritic Cells | IL-12 | IL-6 | CD40 | CD86

Background: T helper 1 and T helper 17 cells play important roles in immunity against foreign invaders. Differentiation of these Th subsets is affected by state of maturation and cytokines that are produced by dendritic cells (DCs). Curdlan is a linear (1→3)-β-glucan and has shown activity against tumors and infectious agents. Objective: This study aims to investigate whether curdlan plays its role through affecting the maturation and cytokine production by DCs. Methods: DCs were isolated from the spleen of BALB/c mice by MACS method. After an overnight culture of DCs in the presence of curdlan, the expression levels of CD40, CD86, and MHC-II molecules were determined by flow cytometry. The production of cytokines involved in Th1 and Th17 cell differen-tiation (IL-12 and IL-6, respectively) was also evaluated by ELISA. Lipopolysaccharide (LPS) treated and untreated cells were considered as positive and negative controls, re-spectively. Results: The results of this study did not show a significant difference in the levels of surface expression of CD40 (p=0.82), CD86 (p=0.79), and MHC class II (p=0.84) molecules upon exposure to curdlan. However, LPS increased the intensity of CD40 expression on dendritic cells (p=0.04). In addition, it was revealed that curdlan-exposed DCs are not able to produce a significant amount of IL-6 and IL-12 cytokines. Conversely, LPS-treated DCs were able to make a significant amount of IL-12 (p=0.005). Conclusion: The results of the present study suggest that curdlan has no ef-fect on Th1 or Th17 differentiation while LPS may induce Th1 deviation by induction of CD40 expression and IL-12 production.

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