Ali Ahmadi; Najmeh Poursasan; Jafar Amani; Jafar Salimian
Volume 12, Issue 1 , March 2015, , Pages 64-69
Abstract
Background: T-2 mycotoxin belongs to the Trichothecene family and has damaging effects on the immune system. Objective: To investigate the toxic effect of T-2 toxin on the percentage of peripheral blood B lymphocytes and the potential protective role of selenium and vitamin E. Method: Frequencies of ...
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Background: T-2 mycotoxin belongs to the Trichothecene family and has damaging effects on the immune system. Objective: To investigate the toxic effect of T-2 toxin on the percentage of peripheral blood B lymphocytes and the potential protective role of selenium and vitamin E. Method: Frequencies of B lymphocytes (CD19+ ) were analyzed after injection of sublethal doses of T-2 toxin into Balb/c mice at different time points, using flowcytometry. Additionally, the effects of selenium and vitamin E on B lymphocyte, as either prophylaxis or simultaneously administered with T-2 toxin, were investigated. Results: After injection of a sublethal dose of T-2 toxin, the number of B cells (CD19+ ) significantly decreased at 12 h and became normal at 72 h. When selenium was injected both 24 h before and simultaneously with T-2 toxin, it was able to inhibit B lymphocyte (CD19+) reduction. In contrast, injecting vitamin E, 24 h before or simultaneously with T-2 toxin did not regulate B lymphocyte alteration. Conclusion: Selenium plays pivotal role on altered B lymphocyte subset induced by T-2 toxin comparing to vitamin E.
Nasrollah Erfani; Mahboobeh Hamedi-Shahraki; Somayeh Rezaeifard; Mohammadreza Haghshenas; Manoochehr Rasouli; Alamtaj Samsami Dehaghani
Volume 11, Issue 2 , June 2014, , Pages 105-112
Abstract
Background: Ovarian cancer is the fifth leading cause of death from malignancy in women. CD4 +CD25+FoxP3+ regulatory T (Treg) cells are a subset of T lymphocytes with great inhibitory impact on immune response. Objectives: To investigate the percentage of CD4 +CD25+FoxP3+ regulatory T cells in the peripheral ...
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Background: Ovarian cancer is the fifth leading cause of death from malignancy in women. CD4 +CD25+FoxP3+ regulatory T (Treg) cells are a subset of T lymphocytes with great inhibitory impact on immune response. Objectives: To investigate the percentage of CD4 +CD25+FoxP3+ regulatory T cells in the peripheral blood of the Iranian patients with epithelial ovarian cancer compared to healthy women and to evaluate the correlation of the Treg cell percentage with clinicopathological characteristics including cancer stage and CA-125 serum level. Methods: Seventeen women with epithelial ovarian cancer and 20 healthy subjects were enrolled in the study. Peripheral blood mononuclear cells were stained at the surface, for CD4 and CD25 molecules, followed by fixation, permeabilization and intracellular staining for FoxP3 molecule. After processing and flowcytometry analysis, prevalence of Treg cells was determined as the percentages of CD25 +FoxP3+ cells among CD4+ lymphocytes. Results: Despite no difference in the percentage of total CD4+ lymphocytes, analysis indicated that Treg cell percentage was significantly higher in ovarian cancer patients than controls (5.7 ± 3.1% versus 2.8 ± 1.4%, p=0.002). A trend toward higher Treg cells was observed in higher stages of ovarian cancer (III+IV) in comparison to lower stages (I+II) (6.5 ± 3.2% vs. 4.44 ± 2.7%, p=0.2). Higher percentage of Treg cells was also observed in the patients with high CA125 (CA-125 >100 U/mL) in comparison to those with low CA-125 serum level (CA-125 ≤100 U/mL) although the difference was not significant (6.44 versus 4.18%, p=0.19). Conclusion: Increased frequency of Tregs in ovarian cancer might participate in immune suppression in these patients. The findings collectively suggest the likely impact of Treg cell–targeted immunotherapy in ovarian cancer.
Abbas Ali Pourazar; Alireza Andalib; Farzad Qreizy; Hadi Karimzadeh; Ahmad Ghavami-Nejad; Behshad Pournasr-Khakbaz
Volume 2, Issue 2 , June 2005, , Pages 91-96
Abstract
Background: Inappropriate activation or blockage of the inhibition of complement system could cause tissue damages in autoimmune diseases particularly rheumatoid arthritis (RA). Defect in complement component regulation may cause damages to tissues, on the other hand, or the damaged tissue might affect ...
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Background: Inappropriate activation or blockage of the inhibition of complement system could cause tissue damages in autoimmune diseases particularly rheumatoid arthritis (RA). Defect in complement component regulation may cause damages to tissues, on the other hand, or the damaged tissue might affect the unnecessary activation of complement components. Objective: To investigate the expression of CD55 and CD 59 complement regulatory proteins in RA patients. Subjects and Methods: Fifty proved rheumatoid arthritis patients participated in this study and their blood were collected for investigations. CD55 and CD59 molecules expression on the erythrocytes was assayed using primary monoclonal antibody and secondary FITC conjugated Ab, then the prepared samples were run with a FACSCalibur flowcytometer (Becton-Dickinson) and the obtained data was analyzed using a Cell Quest software package. To evaluate the complement function, CH50 was performed using patient sera. All experiments were done with a matched healthy volunteer group. Results: The mean fluorescence intensity for CD55 was 27.6 ± 13.4 arbitrary unit for patients and 68.5 ± 10.5 for healthy group. CD59 mean fluorescence intensity was 314 ± 83 in patient group and 508 ± 56 in healthy volunteers. In addition, there was a significant difference between CH50 in patients (54.5 ± 15.5) and in healthy group (110 ± 20). A significant correlation between CD55 and CD59 expansion on the patient erythrocytes was found (P = 0.00, r = 0.576). No association was found between CD59, or CD55 with CH50 (P > 0.05). Conclusion: The expression of CD55 and CD59 is down-regulated on erythrocytes of patients with RA. Change in expression of regulatory complement components in RA may be a useful key for the assessment of disease progression or in patients' follow-up.
