Background and purpose: Several laboratories have developed culture systems including maturation FACTORs for human DC from peripheral blood monocytes. We comprehensively studied the effect of addition of poly (I-C) to standard maturation stimulus, MCM and TNF-a on maturation of monocyte derived DCs and their ability to elicit T cell responses.Materials and methods: A short (4-day) priming of plastic adherent monocytes with granulocytemacrophage colony stimulating FACTOR (GM-CSF) and interleukin-4 (IL-4) followed by allogenic TUMOR antigen pulsing and addition of MCM and TNF-a with or without poly (I-C) to generate fully mature and stable DCs. Phenotypic and functional analysis were carried out using anti CD14, HLA-DR and CD83 monoclonal antibodies, mixed lymphocyte reaction (MLR), phagocytic activity and cytokine release by DC stimulated T lymphocytes.Results: We found that fully matured DCs with large amount cytoplasm and copious dendritic projections were visible at the end of culturing period in the presence of MCM and TNF-a with or without rpoly (I-C). Flow cytometric analysis using anti-CD14, HLA-DR and CD83 revealed that addition of poly (I-C) to conventional maturation FACTORs results in decreased expression of CD14 and increased expression of HLA-DR and CD83. Functionally, MCM and TNF-a with poly (I-C) treated DCs showed a little stronger mixed leukocyte reaction Analysis of phagocytic activity showed that addition of poly (I-C) reduced FITC-conjugated bead uptake and increased mean fluorescent intensity (MFI) of phagocytic DCs. Furthermore our results revealed that additional treatment of DCs with poly (I-C) results in reduction of IL-12: IL-10 and IFN-γ: IL-4 ratios in DC and DC-primed T cell supernatants respectively.Conclusion: Our results support this idea that use of the MCM, TNF-a and poly (I-C) as maturation FACTOR could gnerates more mature monocyte derived DCs that prime T lymphocytes to TH2 type cytokine release.

Introduction: Lichen planus is a skin and mucosal disease with an unknown etiology. However, a number of FACTORs are known to play a role. One of these FACTORs is inflammatory cytokines, such as TNF-α, which play a key role in inflammation. The aim of this study was to evaluate serum levels of TNF-a in patients with oral lichen planus (OLP) and (contact/drug-induced) oral lichenoid reactions (OLR) in comparison with normal controls.Materials and methods: In this descriptive-analytical, cross-sectional study, 10 OLP (mean age 46.84±8.59), 20 OLR patients (mean age 49.18±13.34) and 20 normal controls (mean age 39.86±6.99) were compared and the serum levels of TNF-a were measured by ELISA. Data were analyzed with SPSS 16, using Kruskal-Wallis test (a=0.05).Results: The OLR patients, OLP patients and normal group exhibited no significant differences in the serum levels of TNF-a (p value=0.465). The mean serum levels of TNF-a in OLR and OLP patients and in healthy individuals were 10.45, 30.76 and 50.73, respectively.Conclusion: Under the limitations of the present study, there were no significant differences in the serum levels of TNF-α in patient with OLP and OLR and healthy subjects. Therefore, TNF-a cannot be used to make a distinction between lichen planus and lichenoid reaction lesions.

Background: Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). There is a correlation between up-regulation of a variety of cytokines with inflammatory reactions in multiple sclerosis lesions. This study aimed to investigate the effects of high-intensity resistance exercise program on prevention of experimental autoimmune encephalomyelitis (EAE) (a model for studying multiple sclerosis).Methods: Resistance exercises were performed for 6 weeks, 5 days a week. Training program started with 50% of rats' body weight. In the first session, animals performed 8 to 10 repetitions (up the ladder) with 2-minute rest intervals. Rats were immunized with spinal cord and complete adjuvant of guinea pigs. Disease process and changes in rats' weights were measured every day. Experimental autoimmune encephalomyelitis model was induced at the end of the sixth week of training.Findings: Resistance training in Lewis female rats with experimental autoimmune encephalomyelitis resulted in a significant reduction in TUMOR NECROSIS FACTOR-alpha (TNF-a) (P=0.001) and a significant increase in interleukin-10 (IL-10) (P=0.001). However, it did not cause significant changes in Brain-Derived Neurotrophic FACTOR (BDNF) (P=0.055). In addition, clinical symptoms in exercised rats were postponed.Conclusion: Regarding the results, it appears that resistance exercises with necessary duration and intensity delay the onset, reduce the severity of clinical symptoms, and decrease TNF-a, increase IL-10, with no change in BDNF, in Lewis rats with experimental autoimmune encephalomyelitis.