Maryam Roudbary; Shahla Roudbar Mohammadi; Mahmood Bozorgmehr; Seyed Mohammad Moazzeni
Volume 6, Issue 2 , June 2009, , Pages 67-74
Abstract
Back ground: Candida albicans is a member of the normal human microflora. C. albicans cell wall is composed of several protein and carbohydrate components which have been shown to play a crucial role in C. albicans interaction with the host immune system. Major components of C. albican cell wall are ...
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Back ground: Candida albicans is a member of the normal human microflora. C. albicans cell wall is composed of several protein and carbohydrate components which have been shown to play a crucial role in C. albicans interaction with the host immune system. Major components of C. albican cell wall are carbohydrates such as mannans, β glucans and chitins, and proteins that partially modulate the host immune responses. Dendritic cells (DC), as the most important antigen-presenting cells of the immune system, play a critical role in inducing immune responses against different pathogens. Objective: We investigated the effect of the cell wall protein fraction (CPF) of C. albicans on DC maturation. Methods: The CPF of C. albicans cells was extracted by a lysis buffer containing sodium dodecyl sulphate, 2-mercaptoethanol and phosphate-buffered saline. The extract was dialyzed and its protein pattern was evaluated by electrophoresis. Dendritic cells were purified from Balb/c mice spleens through a three-step method including mononuclear cell separation, as well as 2-h and overnight cultures. The purified CPF was added at different concentrations to DC. The purity and maturation status of DC were determined by flow cytometry using monoclonal antibodies against CD11c, MHC-II, CD40 and CD86. Results: Treatment of DC with 10 μg/ml of CPF increased the expression of maturation markers including MHC-II, CD86 and CD40 on DC compared to the control group. Conclusion: In this study we used C. albicans CPF with the molecular weight of 40-45 kDa for pulsing and maturation of dendritic cells. Since according to our results CPF significantly increased the expression of maturation markers on DC, we suggest that CPF may act as an efficient immunomodulator, or may be used as a potential adjuvant to boost the host immune system against infections.
Hedieh Matloubi; Mohammad Vodjgani; Abbass Ali Nasehi; Mohammad Hossein Niknam; Anoushirvan Kazemnejad; Eisa Salehi; Tahereh Aboufazeli; Zahra Gheflati
Volume 4, Issue 1 , March 2007, , Pages 32-37
Abstract
Background: Apart from genetic and environmental factors, activation of autoreactive mechanisms has been proposed to play a role in the pathogenesis of schizophrenia. In re-cent years, considerable work has been carried out to understand the role and contribution of the immune system in this disease. ...
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Background: Apart from genetic and environmental factors, activation of autoreactive mechanisms has been proposed to play a role in the pathogenesis of schizophrenia. In re-cent years, considerable work has been carried out to understand the role and contribution of the immune system in this disease. Objective: To investigate the T cell response to phytohaemagglutinin (PHA) and determine the serum levels of anti-nuclear antibody (ANA), anti-cytoplasmic antibody (ACA), and circulating immune complexes (CIC) in schizophrenic patients. Methods: A total of 30 drug-free schizophrenic patients and 42 healthy controls were enrolled in this study. T cell proliferation in response to PHA was measured using Methyl Thiazol Tetrazolium test. ANA and ACA were measured by indi-rect immunofluorescence. CIC concentration was determined using poly ethylene glycol precipitation assay. Results: Mean PHA response was 1.96 ± 0.83 in patients and 3.72±1.39 in healthy controls (p < 0.001). ANA and CIC concentrations were not signifi-cantly different between two groups. In addition, ACA was detected only in patients. Conclusion: Increased production of ACA together with lower T cell response to mito-gens in our patients provides evidence for the involvement of autoimmune mechanisms in the pathogenesis of schizophrenia.
