Mohammadreza Yazdani; Shahdad Khosropanah; Ahmad Hosseini; Mehrnoosh Doroudchi
Volume 13, Issue 4 , December 2016, , Pages 249-262
Abstract
Background: Atherosclerosis is a chronic inflammatory disease affecting large and
medium arteries. CD4+ T cells are known to play a role in the progression of the
disease. CD4+CD25+Foxp3+ natural Treg (nTreg) cells seem to have a protective role
in the disease and their reduction in acute coronary ...
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Background: Atherosclerosis is a chronic inflammatory disease affecting large and
medium arteries. CD4+ T cells are known to play a role in the progression of the
disease. CD4+CD25+Foxp3+ natural Treg (nTreg) cells seem to have a protective role
in the disease and their reduction in acute coronary syndrome is recently shown.
Objective: To investigate the frequency of nTreg subsets in the peripheral blood of
patients with atherosclerosis. Methods: Confirmation of atherosclerosis was done by
angiography and 15 ml heparinized blood was obtained from each of the 13 nondiabetic
patients and 13 non-diabetic, non-smoker individuals with normal/insignificant
coronary artery disease which was also confirmed by angiography. Lipid profiles of the
patients and controls were measured at the time of sampling. Mononuclear cells were
used for both RNA extraction and immunophenotyping by real-time PCR and
flowcytometry techniques, respectively. Results: In natural Treg subsets, the frequency
of CD4+CD45RO-CD25+Foxp3lo T-cells (resting nTregs) was greater in controls than
patients (p=0.02). The frequency of CD4+CD45RO+CD25hiFoxp3hi T-cells (activated
nTregs) was significantly higher in controls compared with patients (p=0.02). However,
the frequency of CD4+CD25+CD45RO+Foxp3- T-cells (effector/memory) increased in
patients compared with controls (p=0.01). Both the MFI and gene expression of Foxp3
were higher in control group than in patients (p=0.015 and p=0.017, respectively).
Moreover, the TGF-β gene expression showed a decrease in the peripheral blood
mononuclear cells of patients compared with controls (p=0.03). Conclusion: Decrease
in both subsets of resting and activated nTregs along with a decrease in the expression
of Foxp3 and TGF-β genes in patients with atherosclerosis suggests phenotypic changes
in these subsets, which may as well be correlated with a more inflammatory profile in
their lymphocytes.
Mahboobeh Razmkhah; Nadieh Abedi; Ahmad Hosseini; Mohammad Taghi Imani; Abdol-Rasoul Talei; Abbas Ghaderi
Volume 12, Issue 1 , March 2015, , Pages 1-15
Abstract
Background: Adipose derived stem cells (ASCs) provoke the accumulation and expansion of regulatory T cells, leading to the modulation of immune responses in tumor microenvironment. Objective: To assess the effect of tumoral ASCs on the trend of regulatory T cells differentiation. Methods: Peripheral ...
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Background: Adipose derived stem cells (ASCs) provoke the accumulation and expansion of regulatory T cells, leading to the modulation of immune responses in tumor microenvironment. Objective: To assess the effect of tumoral ASCs on the trend of regulatory T cells differentiation. Methods: Peripheral blood naïve CD4+ T cells were co-cultured with ASCs derived from breast cancer or normal breast tissues. In separate cultures peripheral blood naïve CD4+ T cells were exposed to the culture supernatants of ASCs. Results: Generation of CD4+CD25+Foxp3+ and CD4+CD25- Foxp3+ Treg subsets was observed after coculture of naïve CD4+ T cell with either ASCs or the related supernatant. The percentage of CD4+CD25+Foxp3+ cells increased after exposing naïve CD4+ T cells to both ASCs and their supernatants while augmentation of CD4+CD25-Foxp3+ subset mostly depended on the presence of ASCs. Similarly, upregulation of FoxP3 molecule was more significant in condition of cell to cell contact. IL-4 and IL-10 were up-regulated in the cocultured naïve CD4+ T cells after exposure to ASCs/supernatant while IFN-γ was down-regulated in the presence of ASCs. Conclusion: Accordingly, ASC may act as one of the major players in tumor site with immunomodulatory effects, which may mostly be carried out through direct cellcell interaction.
Zohreh Babaloo; Farhad Babaie; Mehdi Farhoodi; Mohammadreza Aliparasti; Behzad Baradaran; Shohreh Almasi; Ahmad Hosseini
Volume 7, Issue 4 , December 2010, , Pages 1-1
Abstract
Bakground: Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune disease affecting the central nervous system (CNS). It was previously believed that Th1 cells were pathogenic T cells in experimental autoimmune encephalomyelitis (EAE). However, the functional role of Th1 cells in EAE has been reconsidered ...
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Bakground: Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune disease affecting the central nervous system (CNS). It was previously believed that Th1 cells were pathogenic T cells in experimental autoimmune encephalomyelitis (EAE). However, the functional role of Th1 cells in EAE has been reconsidered upon the discovery of IL-17- producing T cells which are consider as dominant effectors for inducing autoimmune tissue inflammation. Objective: The objective of this study was to assess the role of IL-17A and IL-17F in MS pathogenesis. Methods: We evaluated mRNA expression of IL-17A and IL-17F in thirty-five Iranian patients with relapsing–remitting MS (RRMS) and twenty-five healthy controls by Quantitative Real Time PCR. Results: The results of this study showed a twenty-fold increase in the expression of IL-17A mRNA in MS patients compared to the control group (p < 0.0001 ). IL-17F mRNA expression in MS patients was thirty three-times greater than control group (p = 0.0008). IL-17A mRNA expression in periphery was positively correlated with expression of IL-17F transcripts in MS patients and controls (p < 0.01 and p < 0.05, respectively). Conclusion: These results indicate the critical role of Th17- mediated cytokines in development of MS which classically has been considered as a Th1-mediated disorder. The results of this study showed, for the first time, the importance of IL-17F in MS immunopathogenesis.