Multiple sclerosis, a debilitating autoimmune and inflammatory disease of the central nervous system, is associated with both infectious and non-infectious factors. We investigated the role of EBV infection, vitamin D level, and cytokine signature in MS patients. Molecular and serological assays were used to investigate immune biomarkers, vitamin D level, and EBV status in 83 patients with relapsing-remitting multiple sclerosis and 62 healthy controls. In total, 98.8 % of MS patients showed a history of EBV exposure compared to 88.6 % in the healthy group (p = 0.005). EBV DNA load was significantly higher in MS patients than healthy subjects (p < 0.0001). Using a panel of biomarkers, we found a distinct transcriptional signature in MS patients compared to the healthy group with mRNA levels of CD73, IL-6, IL-23, IFN-γ, TNF-α, IL-15, IL-28, and IL-17 significantly elevated in MS patients (p < 0.0001). In contrast, the mRNA levels for TGF-β, IDO, S1PR1, IL-10, and CCL-3 were significantly lower in MS patients compared to healthy controls (p < 0.0001). No significant differences were found with the mRNA levels of IL-13, CCL-5, and FOXP3. Interestingly, in MS patients we found an inverse correlation between vitamin D concentration and EBV load, but not EBNA-1 IgG antibody levels. Our data highlight biomarker correlates in MS patients together with a complex interplay between EBV replication and vitamin D levels.
Common variable immunodeficiency (CVID) is the most frequent symptomatic primary immune deficiency and is characterized by hypogammaglobulinemia, defect in specific antibody response and increased susceptibility to recurrent infections, malignancy and autoimmunity. Patients with CVID often have defects in post-antigenic B-cell differentiation, with fewer memory B cells and impaired isotype switching. Toll-like receptors (TLRs) are expressed on various immune cells as key elements of innate and adaptive immunity. TLR signaling in B cells plays multiple roles in cell differentiation and activation, class-switch recombination and cytokine and antibody production. Moreover, recent studies have shown functional alteration of TLRs responses in CVID patients including poor cell proliferation, impaired upregulation of co-stimulatory molecules and failure in cytokine and immunoglobulin production. The purpose of the present review is to discuss the role of TLRs in B-cell development and function as well as their role in the immunopathogenesis of CVID.
α-Thalassemia (α-thal) is one of the most common inherited hemoglobin (Hb) disorders in the world. In addition to large deletions, over 50 different α-thal point mutations were detected around the world, thus, patients showed different phenotypes with regard to genotype. This study evaluated the genetic frequency of α-thal in Khuzestan Province, Southwest Iran, to help implement premarital and prenatal screening programs. The study was conducted on couples proposing to get married and parents who were referred to the genetic center of Shafa Hospital, Ahvaz, Iran, for prenatal diagnosis (PND) in 2012. Genomic DNA was purified by the salting-out method and tested using multiplex gap-polymerase chain reaction (gap-PCR), amplification refractory mutation system-PCR (ARMS-PCR), reverse hybridization test strips and DNA sequencing. Overall, 11 mutations were found on the α-globin genes. Based on gene frequency, the most common mutant allele was -α(3.7) (rightward) (71.3%) followed by the two gene deletion - -(MED) (9.7%). Other common mutations were α(codon 19)α (GCG>GC-, α2) (8.4%), the polyadenylation (polyA1) site α(polyA1)α (AATAAA>AATAAG) (2.8%), and α(-5 nt)α (-TGAGG) (2.0%). In addition, an extremely rare mutation at α(codon 21)α [Hb Fontainebleau, HBA2: c.64G > C (or HBA1)] was also found. The results of this study are critical for correct diagnosis of α-thal carriers, premarriage counseling and PND. This study suggests that the distribution of mutations on the α-globin genes differs among the ethnic groups in Khuzestan Province as well as in other provinces.
The study evaluates the potential immunocytotoxic effect of aqueous leaf extract of Cassia occidentalis on human peripheral blood mononuclear cells (PBMCs) and Neutrophils. Different concentrations (25 µg/ml, 50 µg/ml, 100 µg/ml) of the extract were prepared. Six millilitres (6ml) of peripheral blood from consented healthy volunteers was collected and PBMCs and neutrophils were isolated on Histopaque media. The viability of PBMCs and neutrophils was determined using trypan blue dye exclusion methods. One-way analysis of variance was used in analysing the results. Total viable cell count (TVCC) for PBMCs and neutrophils yielded 298.9 x 104 cells/ml and 327.9 x 104 cells/ml respectively. The TVCC of the highest concentration (100 µg/ml) of the extract used for the treatment of PBMCs was 192.7 x104 cells/ml and that of neutrophil was 50.47 x104 cells/ml equivalent to 82.51% and 61.71% mean viability percentages respectively. The PBMCs and neutrophils treated with 25 µg /ml of the extract have the highest mean percentage viability scores of 94.88% and 74.61% respectively. There was a significant difference in the mean percentage viability when control PBMCs was compared with those treated with 100 µg/ml (p<0.0001) and also when control neutrophils was compared with those treated with 25 µg /ml (p=0 .02), 50 µg /ml and 100 µg /ml (p<0.0001) respectively. The cell viability tends to decrease in a dose-dependent manner. The aqueous leaf extract of C. occidentalis has a potent cytotoxic effect on both cells, especially at a higher dose. The study recommends an in-depth study to improve the credence of the present study findings. Keywords: Cassia occidentalis extract, Cytotoxic activity, Human Neutrophils and PBMCs
Vitiligo is one of the disease which is yet to understand its pathogenesis, however many studies associate this disease as an autoimmune. Detection of autoimmune cells in the serum, lesional and perilesional area of vitiligo patients gives more insight on the disease mechanism. Presence of autoantibodies against melanocytes antigens in vitiligo patients indicates an autoimmune involvement in the aetiology of the disease. Identification and characterization of vitiligo autoantibodies would pave the way for developing new laboratory test for diagnosis. Studying the autoantibodies profile can give an impression on the disease condition of vitiligo patients. We realized the need of research emphasis in this area as more is yet to be discovered. In this review we give an account on different autoantibodies and their associated autoantigens in vitiligo as another effort of providing an updated data for detail analysis.
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