Rozita Edalat

Pasteur Institute of Iran (IPI), Teheran, Tehrān, Iran

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Publications (3)6.66 Total impact

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    ABSTRACT: Common variable immunodeficiency (CVID) is the most symptomatic primary antibody deficiency associated with recurrent infections and chronic inflammatory diseases as well as autoimmunity. CD4(+) CD25(+) FOXP3(+) regulatory T cells (Tregs) are critical T cell subsets for maintaining self-tolerance and regulation of immune response to antigens thus play a pivotal role in preventing autoimmunity. Thirty seven CVID patients and 18 age-sex matched controls were enrolled. Peripheral blood mononuclear cells (PBMCs) were obtained from both groups and the percentage of Tregs was calculated using flow cytometry method. The mRNA expression of Tregs surface markers cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and glucocorticoid induced tumor necrosis factor receptor (GITR) which are associated with Tregs inhibitory function were compared between patients and controls by quantitative Real-time PCR TaqMan method. The results revealed that the frequency of Tregs was significantly lower in CVID patients than normal individuals (P<0.001). In addition, CVID patients with autoimmunity were found to have markedly reduced proportion of Tregs compared to those cases without autoimmune diseases (P=0.023). A significant difference was seen in FOXP3 expression between CVID patients and controls (P<0.001). The mRNAs of CTLA-4 and GITR genes were expressed at lower levels in CVID patients compared to control group (P=0.005 and <0.001, respectively). Our findings showed reduced proportion of Tregs in CVID patients together with down-regulation of FOXP3 protein and diminished expression of inhibitory Tregs' markers. It could be concluded that all of these changes may be responsible for cellular immune dysregulation observed in these patients especially those with autoimmune manifestation.
    Scandinavian Journal of Immunology 02/2013; · 2.20 Impact Factor
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    [Show abstract] [Hide abstract]
    ABSTRACT: Common variable immunodeficiency (CVID) is the most symptomatic primary antibody deficiency associated with recurrent infections and chronic inflammatory diseases as well as autoimmunity. CD4(+) CD25(+) FOXP3(+) regulatory T cells (Tregs) are critical T cell subsets for maintaining self-tolerance and regulation of immune response to antigens thus play a pivotal role in preventing autoimmunity. Thirty seven CVID patients and 18 age-sex matched controls were enrolled. Peripheral blood mononuclear cells (PBMCs) were obtained from both groups and the percentage of Tregs was calculated using flow cytometry method. The mRNA expression of Tregs surface markers cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and glucocorticoid induced tumor necrosis factor receptor (GITR) which are associated with Tregs inhibitory function were compared between patients and controls by quantitative Real-time PCR TaqMan method. The results revealed that the frequency of Tregs was significantly lower in CVID patients than normal individuals (P<0.001). In addition, CVID patients with autoimmunity were found to have markedly reduced proportion of Tregs compared to those cases without autoimmune diseases (P=0.023). A significant difference was seen in FOXP3 expression between CVID patients and controls (P<0.001). The mRNAs of CTLA-4 and GITR genes were expressed at lower levels in CVID patients compared to control group (P=0.005 and <0.001, respectively). Our findings showed reduced proportion of Tregs in CVID patients together with down-regulation of FOXP3 protein and diminished expression of inhibitory Tregs' markers. It could be concluded that all of these changes may be responsible for cellular immune dysregulation observed in these patients especially those with autoimmune manifestation.
    Scandinavian Journal of Immunology 01/2013; · 2.20 Impact Factor
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    ABSTRACT: Phosphodiesterase 9 (PDE9) is a major isoform of phosphodiesterase hydrolysing cGMP and plays a key role in proliferation of cells, their differentiation and apoptosis, via intracellular cGMP signalling. The study described here was designed to investigate expression, activity and apoptotic effect of PDE9 on human breast cancer cell lines, MCF-7 and MDA-MB-468. Activity and expression of PDE9 were examined using colorimetric cyclic nucleotide phosphodiesterase assay and real-time RT-PCR methods respectively; cGMP concentration was also measured. MTT viability test, annexin V-FITC staining, Hoechst 33258 staining and caspase3 activity assay were used to detect apoptosis. Treatment of both cell lines with BAY 73-6691 lead to reduction in PDE9 mRNA expression, PDE9 cGMP-hydrolytic activity and elevation of the intracellular cGMP response. BAY 73-6691 significantly reduced cell proliferation in a dose- and time-dependent manner and caused marked increase in apoptosis through caspase3 activation. Our results revealed that BAY 73-6691 induced apoptosis in these breast cancer cell lines through the cGMP pathway. These data suggest that BAY 73-6691 could be utilized as an agent in treatment of breast cancer.
    Cell Proliferation 04/2012; 45(3):199-206. · 2.27 Impact Factor