Nicotine Protects Dendritic Cells from Apoptosis and Support DCs-dependent CD4+ T-cell Priming in vitro
By: Tao, X
.
Contributor(s): LI, Hong.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2019Edition: Vol.81(6), Nov-Dec.Description: 1000-1010p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: Dendritic cells are antigen-presenting cells that act as messengers between the innate and adaptive immune systems. Their major function is to process foreign material and present it to CD4+ T-cells. Previous studies have demonstrated that nicotine suppresses the immune function of dendritic cells. However, the role of nicotine on CD4+ T-cells differentiation remains elusive. In this study, the effect of nicotine was examined on the phenotype, activity and apoptosis of murine bone marrow derived dendritic cells, and dendritic cells-dependent differentiation of CD4+ T-cells. It was found that nicotine protected dendritic cells from apoptosis, reduced expression of MHC class II molecular on dendritic cells and the phagocytic, but not endocytic, ability. Moreover, nicotine increased surface co-stimulatory signal markers CD40, CD80 and CD86 in lipopolysaccharide-treated dendritic cells. Dendritic cell-mediated induction of CD4+ T-cells differentiation was evaluated by flow cytometry and q-PCR. Up-regulation of Foxp3, IL-6, IL-10, and IL-13 expression and down-regulating of INF-γ were observed in dendritic cells/CD4+ T-cells co-cultured with nicotine. The nicotine and LPS treatment increased mRNA expression of IL-4, IL-6, IL-13 and decreased INF-γ production and IL-1β mRNA significantly. In contrast, losing sustained nicotine exposure during CD4+ T-cells differentiation, nicotine-pretreated dendritic cells failed to prime native CD4+ T-cells to T helper cells (Th1, Th2, or Treg) for adaptive responses. These findings provide new insights into the immunosuppressive properties of nicotine in dendritic cells, and demonstrate that sustained presence of nicotine protected dendritic cells from apoptosis and play an important role in CD4+ T-cell stimulation and differentiation
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
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Articles Abstract Database
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School of Pharmacy Archieval Section | Not for loan | 2020-2021144 |
Dendritic cells are antigen-presenting cells that act as messengers between the innate and adaptive immune systems. Their major function is to process foreign material and present it to CD4+ T-cells. Previous studies have demonstrated that nicotine suppresses the immune function of dendritic cells. However, the role of nicotine on CD4+ T-cells differentiation remains elusive. In this study, the effect of nicotine was examined on the phenotype, activity and apoptosis of murine bone marrow derived dendritic cells, and dendritic cells-dependent differentiation of CD4+ T-cells. It was found that nicotine protected dendritic cells from apoptosis, reduced expression of MHC class II molecular on dendritic cells and the phagocytic, but not endocytic, ability. Moreover, nicotine increased surface co-stimulatory signal markers CD40, CD80 and CD86 in lipopolysaccharide-treated dendritic cells. Dendritic cell-mediated induction of CD4+ T-cells differentiation was evaluated by flow cytometry and q-PCR. Up-regulation of Foxp3, IL-6, IL-10, and IL-13 expression and down-regulating of INF-γ were observed in dendritic cells/CD4+ T-cells co-cultured with nicotine. The nicotine and LPS treatment increased mRNA expression of IL-4, IL-6, IL-13 and decreased INF-γ production and IL-1β mRNA significantly. In contrast, losing sustained nicotine exposure during CD4+ T-cells differentiation, nicotine-pretreated dendritic cells failed to prime native CD4+ T-cells to T helper cells (Th1, Th2, or Treg) for adaptive responses. These findings provide new insights into the immunosuppressive properties of nicotine in dendritic cells, and demonstrate that sustained presence of nicotine protected dendritic cells from apoptosis and play an important role in CD4+ T-cell stimulation and differentiation
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