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Background: Selenium is an essential trace element with fundamental effects on human biology. Trace elements deficiency is not an uncommon finding in autoimmune diseases. This deficiency may be a consequence of autoimmune diseases or may contribute to their etiology. With regard to evidence showing the association between selenium deficiency and generation of reactive oxygen species and subsequent inflammation, reviewing the role of selenium in collagen vascular diseases could help researchers to devise strategies for managing these diseases., Objective: The present study aimed to evaluate the role of selenium and autoimmune rheumatic diseases., Data Sources: PubMed, Scopus, Science Direct, and Google Scholar., Study Eligibility Criteria: All the studies on the use of selenium without any limitations in terms of the preparation method, administration route, or formulation process were included in the study. The exclusion criteria were: 1) Articles published in languages other than English, 2) Administration of chemical and hormonal drugs rather than selenium, 3) Investigation of the effects of selenium on the autoimmune problems in animal models, and 4) Insufficiency of the presented data or poor description of the applied methods. Furthermore, review articles, meta-analyses, expert opinions, editorial letters, case reports, consensus statements, and qualitative studies were excluded from the study., Data Extraction: In this systematic review, articles were evaluated through searching following keywords in combination with selenium: "autoimmune rheumatic diseases "or "scleroderma" or "systemic sclerosis" or "Behcet's disease" or "Sjögren syndrome" or "systemic lupus erythematosus" or "musculoskeletal diseases" or "rheumatoid arthritis" or "vasculitis" or "seronegative arthritis" or "antiphospholipid antibody syndrome"., Results: Of 312 articles, 280 were excluded and 32 articles were entered in this study. Based on the majority of studies assessing selenium level in patients with collagen vascular diseases, lower selenium levels were observed in these patients. Moreover, the majority of articles showed an improvement in clinical symptoms of collagen vascular diseases compared to controls after the treatment of patients with different dosages of L-selenomethionine., Conclusion: A decrease in the serum level of selenium was noted in patients with autoimmune diseases, which may be a risk factor for inflammation and initiation of autoimmunity in these patients. A sufficient quantity of selenium has been shown to contribute to the management of complications of autoimmune diseases and even improved survival in patients with autoimmune diseases, which may be due to the anti-inflammatory effects of selenium. Since this issue is of clinical importance, it can be considered in potential nutrition interventions and have beneficial effects on some autoimmune diseases., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Systemic lupus erythematosus (SLE) is known as an autoimmune disorder that is characterized by the breakdown of self‐tolerance, resulting in disease onset and progression. Macrophages have been implicated as a factor in the development of SLE through faulty phagocytosis of dead cells or an imbalanced M1/M2 ratio. The study aimed to investigate the immunomodulatory effects of Lactobacillus delbrueckii and Lactobacillus rhamnosus on M1 and M2 macrophages in new case lupus patients. For this purpose, blood monocytes were collected from lupus patients and healthy people and were cultured for 5 days to produce macrophages. For 48 h, the macrophages were then cocultured with either probiotics or lipopolysaccharides (LPS). Flow cytometry and real‐time polymerase chain reaction were then used to analyze the expression of cluster of differentiation (CD) 14, CD80, and human leukocyte antigen – DR (HLADR) markers, as well as cytokine expression (interleukin [IL]1‐β, IL‐12, tumor necrosis factor α [TNF‐α], IL‐10, and transforming growth factor beta [TGF‐β]). The results indicated three distinct macrophage populations, M0, M1, and M2. In both control and patient‐derived macrophage‐derived monocytes (MDMs), the probiotic groups showed a decrease in CD14, CD80, and HLADR expression compared to the LPS group. This decrease was particularly evident in M0 and M2 macrophages from lupus patients and M1 macrophages from healthy subjects. In addition, the probiotic groups showed increased levels of IL‐10 and TGF‐β and decreased levels of IL‐12, IL1‐β, and TNF‐α in MDMs from both healthy and lupus subjects compared to the LPS groups. Although there was a higher expression of pro‐inflammatory cytokines in lupus patients, there was a higher expression of anti‐inflammatory cytokines in healthy subjects. In general, L. delbrueckii and L. rhamnosus could induce anti‐inflammatory effects on MDMs from both healthy and lupus subjects. Significance statement: Macrophages have been implicated as a factor in the development of systemic lupus erythematosus through faulty phagocytosis of dead cells or an imbalanced M1/M2 ratio. The study aimed to investigate the immunomodulatory effects of Lactobacillus delbrueckii and Lactobacillus rhamnosus on M1 and M2 macrophages in new case lupus patients. L. delbrueckii and L. rhamnosus could induce anti‐inflammatory effects on macrophage‐derived monocytes (MDMs) from both healthy and lupus subjects. In both control and patient‐derived MDMs, the probiotic groups showed a decrease in cluster of differentiation (CD) 14, CD80, and Human Leukocyte Antigen – DR expression compared to the lipopolysaccharides (LPS) group. Also observed the increased levels of interleukin (IL)‐10 and transforming growth factor beta and decreased levels of IL‐12, IL1‐β, and tumor necrosis factor α in MDMs from both healthy and lupus subjects compared to the LPS groups. [ABSTRACT FROM AUTHOR]

Background: Systemic lupus erythematous (SLE) and rheumatoid arthritis (RA) are autoimmune diseases in which the antigen-antibody system plays an important role. As blood group and Rh are determined by the presence or absence of antigens on the surface of red blood cells (RBCs), we aimed to determine the distribution of ABO and Rh blood groups in SLE and RA patients and its association with disease manifestations. Methods: This short communication is based on a study that was conducted on 434 SLE and 828 RA patients. We evaluated the distribution of ABO and Rh blood groups in RA and SLE patients. Results: This study projected that in lupus patients, Coombs-positive autoimmune hemolytic anemia and arthritis were more common among the B blood type and Rh-positive group, respectively. Furthermore, there was no relation between ABO and Rh blood group and rheumatoid factor (RF) and anti-Cyclic Citrullinated Peptide (anti-CCP) seropositivity. Moreover, there was no difference in distribution of blood groups in RA and SLE patients. Conclusion: The higher frequency of blood group B in hemolytic anemia, and positive Rh in arthritis in lupus patients, develop the hypothesis of probable role of ABO blood group antigen in some manifestations of lupus. [ABSTRACT FROM AUTHOR]

Several studies have estimated breast cancer risk in patients with systemic lupus erythematosus (SLE) relative to the general population. However, the results have been inconclusive. Therefore, we conducted a meta-analysis to ascertain a more comprehensive conclusion. A systematic literature search of electronic databases including PubMed, Web of Science, Embase, Cochrane Library, and Scopus was conducted to identify eligible studies using multiple search strategies. Based on the degree of heterogeneity, a random-effect model was chosen to calculate the pooled standardized incidence rate (SIR) with 95% confidence interval (CI), to estimate the strength of association between SLE and breast cancer incidence risk. A total of 18 eligible studies including 110,720 patients with SLE were enrolled in this meta-analysis. The combined results showed no significant association between SLE and breast cancer incidence (SIRs = 1.012 (95% CI, 0.797-1.284)). Subgroup analysis by study type, ethnicity, follow-up years, sample size, and SLE diagnostic criteria also showed no altered risk for breast cancer incidence (the summary risk estimate of each subgroup ranged from 0.82 to 1.40 with no statistical significance). This meta-analysis suggests no direct association between SLE and risk of breast cancer incidence. [ABSTRACT FROM AUTHOR]

Autoimmune diseases are characterized by the attack of the immune system to normal tissues. Patients with autoimmune diseases usually have the deficiency of dietary factors that may be related to the etiology of these conditions. Given the role of vitamin E as a physiologic stabilizer of lysosomal membranes, its deficiency can initiate the process of autoimmune diseases or accelerate its progress. It is supposed that vitamin E could reduce oxidative stress, which is an important factor in the pathogenesis of autoimmune diseases. The literature review is indicative of a decrease in the serum levels of vitamin E in almost all autoimmune diseases. Furthermore, there is evidence regarding the possible therapeutic value of vitamin E in the management of autoimmune diseases. Owing to the anti-inflammatory and protective effect of vitamin E against free radicals, and also its important effect on cytokines levels, this vitamin may play a powerful role in the prevention and treatment of rheumatoid arthritis, as well as joint inflammation and damage. Moreover, increased vitamin E intake might decrease the incidence and severity of certain autoimmune diseases through the regulation of the immune system. [ABSTRACT FROM AUTHOR]

This study investigated whether engraftment of MSCs helped prevent or alleviate the clinical course of SLE in a model of induced lupus by Pristane (as an adjuvant in humanized vaccines). MSC-based immunotherapy had a significant delaying effect on acquired SLE disease progression in a treatment-stage-dependent manner without immunosuppressive drug-related cytotoxicity. By modulating T -cell differentiation and promoting cytokine balance, MSCs, as a new treatment option, have shown promising therapeutic potential for this purpose, which may lead to delayed lupus autoimmunity through the paracrine loop or by direct interaction. The effectiveness of allogeneic MSCs transplantation in delaying disease progression in this preclinical study supports the view that in future prospects of MSCs in SLE, manipulation of their immunomodulatory function can make them an ideal treatment in the amplification of immunological tolerance. The conflicting results of early versus advanced therapy suggest that MSCs may produce different effects depending on when they are administered and their activation status. In the future, it will be important to learn when MSCs exert the best therapeutic effects in autoimmune disorders and to understand the cross-talk between MSCs and target cells in different conditions. [Display omitted] Despite advances in general and targeted immunosuppressive therapies, limiting all mainstay treatment options in refractory systemic lupus erythematosus (SLE) cases has necessitated the development of new therapeutic strategies. Mesenchymal stem cells (MSCs) have recently emerged with unique properties, including a solid propensity to reduce inflammation, exert immunomodulatory effects, and repair injured tissues. An animal model of acquired SLE mice was induced via intraperitoneal immunization with Pristane and affirmed by measuring specific biomarkers. Bone marrow (BM) MSCs were isolated from healthy BALB/c mice and cultured in vitro , then were identified and confirmed by flow cytometry and cytodifferentiation. Systemic MSCs transplantation was performed and then several parameters were analyzed and compared, including specific cytokines (IL-17, IL-4, IFN-ɣ, TGF-β) at the serum level, the percentage of Th cell subsets (Treg/Th17, Th1/Th2) in splenocytes, and also the relief of lupus nephritis, respectively by enzyme-linked immunosorbent assay (ELISA), flow cytometry analysis and by hematoxylin & eosin staining and also immunofluorescence assessment. Experiments were carried out with different initiation treatment time points (early and late stages of disease). Analysis of variance (ANOVA) followed by post hoc Tukey's test was used for multiple comparisons. The rate of proteinuria, anti-double-stranded deoxyribonucleic acid (anti-dsDNA) antibodies, and serum creatinine levels decreased with BM-MSCs transplantation. These results were associated with attenuated lupus renal pathology in terms of reducing IgG and C3 deposition and lymphocyte infiltration. Our findings suggested that TGF-β (associated with lupus microenvironment) can contribute to MSC-based immunotherapy by modulating the population of TCD4+ cell subsets. Obtained results indicated that MSCs-based cytotherapy could negatively affect the progression of induced SLE by recovering the function of Treg cells, suppressing Th1, Th2, and Th17 lymphocyte function, and downregulating their pro-inflammatory cytokines. MSC-based immunotherapy showed a delayed effect on the progression of acquired SLE in a lupus microenvironment-dependent manner. Allogenic MSCs transplantation revealed the ability to re-establish the balance of Th17/Treg, Th1/Th2 and restore the plasma cytokines network in a pattern dependent on disease conditions. The conflicting results of early versus advanced therapy suggest that MSCs may produce different effects depending on when they are administered and their activation status. [ABSTRACT FROM AUTHOR]

Immunoglobulin G4-related disease (IgG4-related disease) is a fibroinflammatory disorder defined by elevated serum IgG4 level and plasma cells tissue infiltration accompanied by fibrosis or sclerosis. In this article, we report two patients of IgG4 syndrome: a 60-year-old male with complaints of nasal congestion, rhinitis, anosmia and hearing loss, and a 28-year-old female with bilateral orbital and parotid gland swelling. Histopathological findings and high serum IgG4 level confirmed diagnosis of IgG4-related disease. Both patients were treated successfully with glucocorticoids and methotrexate. Herein, we also review clinical presentations of IgG4-related disease in head and neck, and related diagnostic and therapeutic approach. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is an autoimmune disease in which polymorphisms within the human leukocyte antigen (HLA) region have been associated to its etiology. We conducted this study to compare the HLA-DQB1 allelic sequence variation among SLE patients and controls in the northeast of Iran. Genomic DNA of 40 SLE patients and 83 healthy controls were amplified by Polymerase Chain Reaction with Sequence-Specific Primers technique (PCR-SSP). Seven serological subclasses of the HLA DQB1 were detected. Allele distribution comparison showed in the SLE group a significant increase of HLA DQ6 (*0601-*0609) (p=0.006); whereas alleles HLA DQ7 (*0301-*0304) were significantly decreased (p=0.005). Combination of DQ5 (*0501-*0504)-DQ6 (*0601-*0609) was increased in patients. These results suggest that DQ6 is the dominant HLA DQB1 allele probably associated with genetic susceptibility to SLE in the northeast of Iran. The association supports the importance of ethnic background and indicates the importance of various genes that has been observed in different SLE populations. [ABSTRACT FROM AUTHOR]

Aim: Rheumatoid arthritis (RA) is the most common chronic inflammatory erosive joint disease with the worldwide distribution of approximately 0.5–1.0%. Etiology of RA is not exactly known but immunologic and genetic factors play an important role in the pathogenesis of the disease. Genetic factors such as human leukocyte antigens (HLA) are responsible for many autoimmune diseases; therefore we decided to look for a correlation between RA and the presence of HLA-DQβ1 alleles as possible genetic markers. Methods: Genomic DNA from the whole blood samples of 25 patients with RA and 86 normal individuals as control group were extracted by salting out method. The genomic DNA was amplified by polymerase chain reaction-sequence specific primer (PCR-SSP) technique. HLA-typing was done by this method after optimizing the PCR reaction for each allele. In this procedure seven serological subclasses of HLA-DQβ1 can be detected. Results: Comparing the results between the patients and controls show a significant increase in the frequency of HLA-DQ8 (*0302, *0305) alleles in RA patients. The P-values were 0.007 and the relative risk for these alleles was evaluated higher than 1. Conclusions: The results suggest that DQ8 is the dominant HLA-DQβ1 allele that is associated with susceptibility to RA in north-eastern Iran. [ABSTRACT FROM AUTHOR]

Several data link vitamin D to many autoimmune diseases. Association between vitamin D receptor (VDR) gene BsmI polymorphisms and systemic lupus erythematosus has been reported. In this study, we examine whether the VDR gene BsmI polymorphisms are markers for susceptibility to or severity of SLE. This study incorporated 60 patients with SLE living in northeastern Iran. Three genotypes, BB, Bb and bb, were detected based on polymerase chain reaction–restriction fragment length polymorphism (PCR/RFLP). The distribution of VDR genotyping in patients with SLE was 23.3% for BB, 60% for Bb and 16.7% for bb and in the control group was 33.3% for BB, 46.7% for Bb and 20% for bb ( P = 0.334). No association of VDR gene BsmI polymorphisms with SLE disease activity index (SLEDAI), SLE damage score and major organ involvement was detected. The result of this study did not show any association between VDR gene BsmI polymorphisms and SLE. [ABSTRACT FROM AUTHOR]

Background: Soluble Fas (sFas) is a marker of apoptosis that appears to increase in the serum of systemic lupus erythematosus patients and may have a correlation with disease activity. The exact role of sFas in apoptosis is not clear. The purpose of this study is to assess the correlation between serum levels of soluble Fas (Apo/1-CD95) and the activity of systemic lupus erythematosus. Patients and Methods: Our study was performed on 114 systemic lupus erythematosus patients who were compared with 50 randomly selected sex, age and race-matched healthy controls. Disease activity was defined according to the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI-2K). All physical exams and laboratory parameters were collected to determine the SLEDAI. sFas levels were determined using a commercially available ELISA kit. Results: There was a significant difference between serum levels of sFas in the case and control groups (P=0.001). A significant correlation coefficient existed between the sFas and SLEDAI2K variables (P=0.001, r=0.494). Significant statistical difference was found between serum levels of sFas in the active and inactive phases of disease according to SLEDAI= 9 or≥10, (P=0.002). The sFas levels were 270 - 300 pg/mL for SLEDAI≤9 and 355-502 pg/mL for SLEDAI≥10, with a confidence interval of 95%. Conclusion: This study shows a significant elevation of sFas levels in the sera of systemic lupus erythematosus patients with active disease; therefore it can be used as an appropriate marker for evaluation of disease activity. [ABSTRACT FROM AUTHOR]