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Premature ovarian failure is a to some extent unknown and intricate problem with diverse causes and clinical manifestations. The lack of ovarian sex hormones presumably is effective in the occurrence of ovarian failure. Our progress in this field has been very little despite undertaken scientific research endeavors; scholars still are trying to understand the explanation of this dilemmatic medical condition. In contrast, the practice of clinical medicine has made meaningful strides in providing assurance to the women with premature ovarian insufficiency that their quality of life as well as long-term health can be optimized through timely intervention. Very recently Scientists have investigated the regulating effects of small RNA molecules on steroidogenesis apoptosis, ovulation, gonadal, and corpus luteum development of ovaries. In this literature review, we tried to talk over the mechanisms of miRNAs in regulating gene expression after transcription in the ovary. 9nPs_Ypm2yRV7ZYy5cg5NU Video abstract [ABSTRACT FROM AUTHOR]

Present research was performed to assess the effects of nanocurcumin supplementation on T‐helper 17 (Th17) cells inflammatory response in patients with Behcet's disease (BD). In this randomized double-blind, placebo-controlled trial, 36 BD subjects were randomly placed into two groups to take 80 mg/day nanocurcumin or placebo for eight weeks. Disease activity, frequency of Th17 cells and expression of related parameters including retinoic acid‐related orphan receptor γ (RORγt) transcription factor messenger RNA (mRNA), related microRNAs (miRNAs) such as miRNA-155, miRNA-181, and miRNA-326 as well as proinflammatory cytokines including interleukin (IL)‐17 and IL‐23 were evaluated. Thirty-two patients (17 in the nanocurcumin and 15 in the placebo groups) completed the trial. Number of Th17 cells decreased significantly in the nanocurcumin group compared to baseline (p =.012) and placebo (p =.047). Moreover, RORγt, IL‐17, IL‐23, miRNA-155, miRNA-181, and miRNA-326 mRNA expression decreased significantly in the nanocurcumin group compared with baseline (p =.004, p =.009, p <.001, p <.001, p <.001, p <.001, respectively) and placebo (p =.002, p =.021, p =.006, p =.035, p <.001, p =.017, respectively). Significant reductions in IL-17 and IL-23 were seen in nanocurcumin group compared with baseline (p =.017 and p =.015) and placebo (p =.047 and p =.048, respectively). Significant reduction in disease activity was observed in nanocurcumin group compared with placebo group (p =.035). Nanocurcumin supplementation had favorable effects in improving inflammatory factors and disease activity in BD patients. Additional studies are warranted to suggest nanocurcumin as a safe complementary therapy in BD. Nanocurcumin supplementation decreased Th17 cells frequency significantly compared with baseline and placebo group. Nanocurcumin supplementation decreased mRNA expression of RORγt, IL‐17, IL‐23, miRNA-155, miRNA-181, and miRNA-326 significantly compared to baseline and placebo group. Nanocurcumin supplementation decreased cell supernatant IL-17 and IL-23 significantly compared to baseline and placebo group. Nanocurcumin supplementation decreased disease activity significantly compared to placebo group. [ABSTRACT FROM AUTHOR]

As critical mediators in biological processes, microRNAs (miRNAs) which are small and endogenous noncoding RNAs have been associated with disease progression, cell proliferation, and development. Pre‐eclampsia (PE), a pregnancy‐related disorder with no early markers or symptoms is recognized as the main reason for fetal and maternal mortality and morbidity in the initial steps or even during pregnancy, worldwide. Clinical symptoms usually appear in the third trimester of the pregnancy. Although numerous research have unraveled several aspects of placenta development abnormalities associated with abnormal trophoblastic invasion and angiogenesis modification, many questions about the PE pathogenesis remains unanswered. A large number of studies have shown the important role of miRNAs as potential biomarkers in the PE prognosis and diagnosis. Here, the latest investigations about the PE and placental miRNAs expression, as well as, the crucial role of miRNA molecules including miR‐210 and miR‐155 which are deregulated in patients with PE, will be argued. [ABSTRACT FROM AUTHOR]

Slow coronary flow (SCF) is a coronary artery disorder. Several inflammatory mediators have been reported to be associated with vascular homeostasis and endothelial dysfunction. The aim of this study was to investigate the association between cytokines and miRNAs in patients with SCF compared to the controls. In this regard, blood samples were acquired from 45 SCF patients and 45 age- and sex-matched healthy control subjects. Serum and peripheral blood mononuclear cells (PBMCs) were separated. Expression levels of miRNAs and cytokines in PBMCs were measured by real-time PCR. As a final point, serum levels of cytokines were quantified by ELISA. Expression levels of miR-1, miR-133, miR-208a, miR-206, miR-17, miR-29, miR-223, miR-326, and miR-155 as considerable indicators of inflammatory function significantly increased in SCF patients while the expression levels of miR-15a, miR-21, miR-25, miR-126, miR-17, miR-16 and miR-18a as considerable indicators of anti-inflammatory function significantly decreased in patients with SCF compared to the control group. Additionally, serum IL-1β, IL-8, and TNF-α concentrations were significantly higher in the SCF group than controls. However, no significant differences were observed in IL-10 production in SCF patients compared to the controls. This study provided the potential role of miRNAs as biomarkers for SCF diagnosis as well as suitable markers for monitoring coronary artery disease (CAD) development in these patients. More investigations are still necessary to unravel the detailed essential mechanisms of circulating miRNA levels in patients with heart failure and SCF. [ABSTRACT FROM AUTHOR]

Preeclampsia (PE) is a disorder affecting 2–10% of pregnancies and has a major role for perinatal and maternal mortality and morbidity. PE can be occurred by initiation of new hypertension combined with proteinuria after 20 weeks gestation, as well as various reasons such as inflammatory cytokines, poor trophoblast invasion can be related with PE disease. Environmental factors can cause epigenetic changes including DNA methylation, microRNAs (miRNAs), and histone modification that may be related to different diseases such as PE. Abnormal DNA methylation during placentation is the most important epigenetic factor correlated with PE. Moreover, changes in histone modification like acetylation and also the effect of overregulation or low regulation of miRNAs or long noncoding RNAs on variety signaling pathways can be resulted in PE. The aim of this review is to describe of studies about epigenetic changes in PE and its therapeutic strategies. [ABSTRACT FROM AUTHOR]

Epithelial–mesenchymal transition (EMT) is a phenomenon in which epithelial cells lose their cell‐to‐cell connection and are detached from the base membrane. EMT is fundamental for many biological processes such as embryonic development and neurogenesis. It also plays a significant role in cancer progression and metastasis. EMT regulation occurs through a sophisticated network of transcription regulations that include many signaling pathways. The exact mechanism of cancer gene regulation has not been understood yet. However, it is interesting to study the role of microRNAs and epigenetics mechanism in the cancer development. In this review, the transcription regulation of EMT and the analysis of possible overlap between microRNAs and their targets which are involved in the cancer development are scrutinized. In nature, MT participates in many physiological and pathological processes including embryonic development, organogenesis, wound healing, and cancer metastasis. Many aspects regulate EMT including: transcription factors, gene expression patterns, and signaling pathway crosstalk. MicroRNAs as noncoding genes play a distinct role in the progression or suppression of EMT. [ABSTRACT FROM AUTHOR]

Problem: Inappropriate activation of the immune system, particularly the imbalance of T‐helper type 17 (Th17)/regulatory T (Treg) cells is thought to play considerable roles in preeclampsia (PE). To investigate the probable effects of the adaptive immune system in the pathophysiology of PE, we analyzed the dynamic changes of Th17/Treg cells, cytokines profile, and transcription pattern of Th17/Treg‐related genes and microRNAs (miRNAs) in 50 women suffering from PE in comparison with 50 healthy pregnant women. Methods: Expressions of cytokines, specific transcription factors, and related miRNAs were measured by real‐time polymerase chain reaction (PCR). Enzyme‐linked immunosorbent assay (ELISA) was used to test the interleukin (IL)‐17, IL‐23, IL‐6, and IL‐10 and transforming growth factor β in serum and supernatant of peripheral blood mononuclear cells (PBMCs). The frequency of Th17 and Treg cells were determined by flow cytometry. Results: PE patients exhibited a decreased number of Treg cells (p = 0.006), while Th17 cells were increased (p = 0.004). Forkhead box P3 and IL‐10 mRNA expressions were reduced (p = 0.0001 and 0.0028, respectively), while expressions of retinoic acid receptor‐related orphan nuclear receptor γt, IL‐17, IL‐23, and IL‐6 were enhanced (p < 0.0001, 0.0018, 0.0014, and 0.027, respectively). ELISA results also showed increased levels of IL‐6, IL‐17, and IL‐23 (p = 0.022, 0.0005, 0.0081, respectively), and decreased levels of IL‐10 in the supernatant of PBMCs of PE patients compared with control group (p = 0.0011). There was significant upregulation of miR‐106b and miR‐326 (p = 0.0048 and 0.028, respectively) in PE patients in comparison with the control group. Conclusions: These findings suggest that imbalance of Th17/Treg cells, regulated possibly via microRNAs, may be involved in the pathogenesis of PE, emphasizing on the importance of these cells in feto‐maternal immune cross‐talk. Inappropriate activation of the immune system, particularly the imbalance of T‐helper type 17/regulatory T cells is thought to play considerable roles in preeclampsia. [ABSTRACT FROM AUTHOR]

Impaired inflammatory immune cells have been implicated in the pathogenesis of Behcet's disease (BD). In the current study, we aimed to evaluate the frequency of T helper (Th) 17 and regulatory T (Treg) cells, cytokine secretion, the expression of transcription factors related to Th17 and Treg cells, and microRNAs (miRNAs) targeting these transcription factors in BD patients. Blood samples from 47 BD patients and 58 healthy subjects were drawn, and the peripheral blood mononuclear cells (PBMCs) were separated and isolated. The frequency of Th17 and Treg cells was assessed using flow cytometry. Transcription factors related to these cells and miRNAs targeting these transcription factors were quantified using real‐time polymerase chain reaction. Finally, the levels of associated cytokines were measured using enzyme‐linked immunosorbent assay. A significant reduction in the percentage of Treg cell frequency and the levels of interleukin (IL)‐10 and forkhead box P3 messenger RNA (mRNA) expressions were observed. The proportion of Th17 cells was notably increased, which was accompanied by a increased levels of IL‐17, IL‐23, and retinoic acid‐related orphan receptor ɣ (RORɣt) mRNA expressions in BD patients. The level of Th17‐associated cytokines in the supernatant was found to be elevated in BD patients. T‐cell‐associated miRNA expression levels, miR‐25, miR‐106b, miR‐326, and miR‐93 were significantly upregulated, while miR‐146a and miR‐155 levels were lower in PBMCs of patients with BD when compared with the controls. The increase in the proportion of Th17 cells alongside the decrease in Treg cells are possibly the involving factors in the pathogenesis of BD. Therefore, the evaluation of immune cells and related miRNA profile may serve as both prognostic biomarker and therapeutic approach in treating patients with BD. [ABSTRACT FROM AUTHOR]

Recurrent pregnancy loss (RPL) is a multifactorial disorder of women in reproductive age, which in some cases is caused by immunologic abnormalities. In this study, we aimed to evaluate cellular and molecular components of the immune system like different T‐cell subsets and their regulating microRNAs (miRNAs) in RPL women and control group. Fifty RPL and 50 healthy subjects were recruited. Subsets of T cells, including regulatory T (Treg) cells, helper T (Th) 17 cells, exhausted T cells, exhausted Treg cells were evaluated by flow cytometry. Transcription factors of T cells and related miRNA profile were quantified using real‐time polymerase chain reaction (RT‐PCR). Assessment showed that Treg and exhausted T cells, were decreased in RPL patients (p = 0.009 and 0.02, respectively), while an increase was observed in Th17 and exhausted Treg frequency (p = 0.013 and 0.0037, respectively). Messenger RNA expression level of T‐bet and IRF4 was upregulated in RPL patients (p = 0.011 and 0.0001, respectively), while Th2‐ and Treg‐related transcription factors, GATA3 and GITR, were downregulated in these patients compared with the healthy subjects (p = 0.0008 and <0.000, respectively). Treg‐associated miRNAs, the miR‐106b‐25–93 cluster, showed a higher rate in RPL patients (P = 0.007, 0.001, and 0.029, respectively), however, we observed no significant difference in the expression level of Th17‐associated miRNA, mir‐326. According to the results, we concluded that unbalanced immune responses and deregulated function of T‐cell subsets may lead to reproduction‐related failure like a miscarriage. Therefore, evaluation of immune cells and related miRNA profile may serve as prognostic biomarker for the treatment of RPL patients. Balanced immune responses are required for a successful pregnancy therefore lack of suppressor mechanisms and increased inflammatory parameters may negatively affect the pregnancy. [ABSTRACT FROM AUTHOR]

In the current study, we aimed to identify nanocurcumin effects on microRNAs (miRNAs) in the peripheral blood of patients with relapsing‐remitting multiple sclerosis (RRMS). We intended to investigate the expression pattern of these miRNAs in experimental settings in vivo. The expression levels of the selected 27 miRNAs known to be involved in the regulation of immune responses were analyzed in 50 RRMS patients and 35 healthy controls. The miRNA expression profiles were investigated by quantitative PCR (qPCR) at baseline and after 6 months of nanocurcumin therapy. Our data revealed that the expression of a number of microRNAs including miR‐16, miR‐17‐92, miR‐27, miR‐29b, miR‐126, miR‐128, miR‐132, miR‐155, miR‐326, miR‐550, miR‐15a, miR‐19b, miR‐106b, miR‐320a, miR‐363, miR‐31, miR‐150, and miR‐340 is regulated by nanocurcumin. The results of the current work indicate that nanocurcumin is able to restore the expression pattern of dysregulated miRNAs in MS patients. We discovered that some miRNAs are deregulated in untreated patients compared with healthy controls and nanocurcumin‐treated patients. This is a new finding that might represent the potential contribution of these miRNAs to MS pathogenesis. Taken together, these data provide novel insights into miRNA‐dependent regulation of the function of B and T cells in MS disease and enrich our understanding of the effects mediated by a therapeutic approach that targets B and T cells. [ABSTRACT FROM AUTHOR]

Lack of regulation of microRNAs (miRNAs) expression has been observed in some autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus. G2013, as a novel non-steroidal anti-inflammatory drug (NSAID) with the immunomodulatory property, has been shown the positive effects in multiple sclerosis and anti-ageing experimental models. This research aimed to study the inhibitory effect of G2013 on miR-155 gene expression using HEK-Blue hTLR4 and Null2 cell lines. Total RNA was extracted from the treated and control cells. cDNA was made for miRNA and expression levels of miR-155 were detected by quantitative Real-time PCR using a specific primer together with U6 as the internal reference gene. A non-significant reduction was observed in the gene expression level of miR-155 in the HEK-Blue hTLR4 and Null2 cell lines under the influence of a low dose of G2013. In contrast, adding lipopolysaccharide (LPS) to the mentioned cells led to a significant increase in miR-155 expression, whereas addition of LPS four hours after exposing the cells with G2013 could not increase the expression level of this miRNA (P < 0.05). Collectively, this research showed that G2013, as a novel NSAID with immunomodulatory property is able to significantly decrease the gene expression of miR-155 following stimulation by LPS. [ABSTRACT FROM AUTHOR]

• Ozone therapy has anti-oxidant and anti-inflammatory therapeutic functions. • Ozone therapy is known as a useful and potential therapeutic approach. • Th17 cell and its related factors have a critical role in MS pathogenesis. • Ozone autohemotherapy could lower the Th17 responses in MS patients. • Ozone autohemotherapy can be a beneficial treatment in MS patients. : Multiple sclerosis (MS) is a neurodegenerative autoimmune disease with chronic inflammation. In the course of the disease, the increased levels of Th17 cell, and its relevant inflammatory factors, may cause disease inflammation and progression. Ozone therapy with anti-oxidant and anti-inflammatory functions is known as a beneficial therapeutic approach. The current non-controlled study aimed to evaluate the therapeutic implications of ozone autohemotherapy on Th17 responses in MS patients. : 20 MS patients as the experimental group received ozone therapy (100 ml of O2/O3 compound (25 ugs/ml concentration) with 100 ml of autologous blood) twice per week for 6 months. The frequency of Th17 cells, gene expression of the relevant factors (RORɣt, IL-17, IL-23, miR-141, miR-155, and miR-200), as well as the secretion levels of IL-17 and IL-23 cytokines, were compared between the patient and control groups, as well as the group of patients before and after ozone therapy using the flow cytometry, Real-time PCR, and ELISA techniques, respectively. : Findings indicated the significant decrease in the frequency of Th17 cells (P = 0.0002), the expression levels of RORɣt and IL-17 (P = 0.0001 and P = 0.0004, respectively), as well as miR-141 and miR-155 (P <0.0001 and P <0.0001, respectively) in post-treatment condition with Ozone compared to pre-treatment condition. Also, the significant reduction in the secretion level of IL-17 (P = 0.043) was detected in treated patients. : Since increased levels and responses of Th17 cells may have critical roles in MS pathogenesis and inflammation, our findings revealed that ozone autohemotherapy could lower the Th17 responses in peripheral blood of MS patients and can be a beneficial approach in MS treatment. [ABSTRACT FROM AUTHOR]

Problem: Increased oxidative stress (OS) and inflammatory factors in metabolic syndrome (MS) patients are considered as risk factors for recurrent implantation failure (RIF). The aim of this study was to investigate OS markers, inflammatory factors, related microRNAs (miRNA) expression, and cytokine and transcription factors RNA expression. Method of study: We evaluated the frequency of helper T (Th) 17 and regulatory T (Treg) cells in recurrent implantation failure (RIF) women with or without MS. miRNA expression, an inflammatory cytokine, and transcription factors were measured by real‐time PCR. The level of interleukin (IL)‐1β, IL‐6, IL‐17, tumour necrosis factor‐alpha (TNF‐alpha) and chemokine (C‐C motif) ligand 2 (CCL‐2), and C‐X‐C motif chemokine ligand 8 (CXCL‐8) were measured by enzyme‐linked immunosorbent assay (ELISA). OS markers were evaluated by spectrophotometric assay. Th17 and Treg cell frequencies were determined by flow cytometry. Results: The expression of AP1, NF‐κB, FOXP3, miRNA‐21; serum or plasma level of OS markers (ie, nitric oxide, total oxidant status, and myeloperoxidase); serum level of inflammatory factors (ie, IL1‐β, IL‐6, IL‐17, TNF‐alpha, CXCL‐8, and CCL‐2); and frequency of Th17 cells were increased in RIF‐MS patients in comparison with RIF women without MS (RIF‐NMS) and control group. The expression of miRNA‐223 and 146a, antioxidant enzymes, namely superoxide dismutase (SOD) and catalase (CAT), and frequency of Treg also declined in RIF‐MS patients. Conclusion: Overall, our findings suggest that MS in RIF patients causes increased inflammatory factors and OS, which in turn leads to implantation failure. [ABSTRACT FROM AUTHOR]

Abstract Biosensors have been commonly used in biomedical diagnostic tools in recent years, because of a wide range of application, such as point-of-care monitoring of treatment and disease progression, drug discovery, commonly use food control, environmental monitoring and biomedical research. Additionally, development of DNA biosensors has been increased enormously over the past few years as confirmed by the large number of scientific publications in this field. A wide range of techniques can be used for the development of DNA biosensors, such as DNA nano-machines and various signal amplification strategies. This article selectively reviews the recent advances in DNA base biosensors with various signal amplification strategies for detection of cancer DNA and microRNA, infectious microorganisms, and toxic metal ions. Highlights • Biosensor technology solves some problems regarding to low sensitivity, time, and cost issues in clinical diagnosis. • Biosensors are employed in disease monitoring, drug discovery, detection of pollutants, disease-causing microorganisms and markers in bodily fluids. • The acid biosensors have been considered for genetic therapy, cancer screening, molecular diagnosis, and environmental monitoring. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is a chronic and organ-specific autoimmune disease in which immune cells act against the myelin sheath, resulting in central nervous system (CNS) damage. It has been revealed that miRNAs can play significant role in the pathogenesis of MS. These regulatory molecules lead to the activation of different signaling pathways, regulation of several transcriptional factors, influencing the differentiation of Th17 cells, development of Tregs and alteration from Th2 to Th1 response in MS. New studies have discovered that dysregulation of miRNAs may trigger abnormal immune responses leading consequently in the emergence of autoimmunity. In this review, we have discussed the altered expression patterns of miRNAs discovered in MS patients. These types of dysregulated miRNAs have been associated with MS pathogenesis. Current outcomes propose that such dysregulated miRNAs are potential to serve as useful biomarkers to diagnose MS, and to recognize new healing targets for its treatment. [ABSTRACT FROM AUTHOR]

The molecular mechanisms involved in the pathogenesis of recurrent pregnancy loss (RPL) are not completely recognized. The present study aimed to assess the molecules associated with ATP catabolism and hypoxia besides their related miRNAs in patients with RPL. The frequency of Th17 and Treg cells in PBMCs of RPL women and healthy pregnant women were evaluated with Flow cytometry. The expression levels of CD39, CD73, and Hypoxia-inducible factor-alpha (HIF-1α), miR-18a, miR-30a, and miR-206 in PBMCs of two groups were measured with real-time PCR and western blotting. Then, serum levels of IGF-1, TGF-β, and HIF-1α were measured by ELISA. Our results indicated a higher (p = 0.0002) and lower (p < 0.0001) frequency of Th17 and Treg lymphocytes in RPL women, respectively. The expression level of CD39 decreased in PBMCs of RPL women whereas the level of CD73 and HIF-α increased (p = 0.0010, 0.0023, 0.0006 respectively). The results of CD39 and CD37 were also confirmed by protein analysis (p = 0.0047, 0.0364 respectively). Almost, the same results for CD39 and CD73 expression at mRNA and protein levels were observed in isolated Treg cells. Moreover, we found the higher expression of miR-206 and miRNA-30a (p = 0.0038, 0.0123), but the lower expression of miRNA-18a (p = 0.0101) in RPL. The concentration level of IGF-1, and TGF-β reduced (p = 0.0017, 0.0065 respectively) while the level of HIF-α elevated (p = 0.0235) in serum samples of RPL. In conclusion, we observed the dysregulation of molecules that are involved in ATP catabolism and hypoxia, including CD39, CD73, and HIF-1a which is related to miR-18a, miR-30a, and miR-206 change in RPL women. It may be potentially used for RPL prognosis by more comprehensive future studies. • The molecular mechanisms are involved in the pathogenesis of RPL are not completely recognized. • Dysregulation of molecules that are involved in ATP catabolism and hypoxia is observed in RPL. • miR-18a, miR-30a, and miR-206 expression changes are altered hypoxia and ATP catabolism condition in RPL patients. [ABSTRACT FROM AUTHOR]

Breast cancer, the most common cancer among women, is a heterogeneous and complex disease, which detail of its precise progression mechanisms is less understood. So, an improved comprehension of the precise molecular mechanisms leading to disease progression and design of effective targeted therapies are required for patients with breast cancer. MicroRNAs demonstrate an uncovered class of small and endogenous non-coding RNAs and play an important role in the normal biological processes, including cell differentiation, proliferation and apoptosis. Some miRNAs, known as oncomiR, show different expression levels in cancer and are capable to effect on cellular transformation, carcinogenesis and metastasis and are characterized by high expression levels in tumors compared to normal tissues. Therefore, oncomiRs can be considered as prognostic biomarkers and therapeutic targets in different types of cancers. Moreover, the utilization of oncomiRs as therapeutic targets for cancer is promising. Accordingly, there is evidence which implies an important role of various oncogenic microRNAs in immunopathogenesis of breast cancer. In this review we will discuss about the role of various oncomiRs such as miR-21, miR-155, miR-10b, and miR-221/222 in the pathogenesis and treatment of breast cancer. [ABSTRACT FROM AUTHOR]

Drug resistance remains one of the major reasons of therapy failure in gastric cancer patients. Although the mechanisms of anticancer drug resistance have been broadly investigated, they have not been completely understood. Accumulating reports have recently highlighted the involvement of endogenous non-coding RNAs, known as microRNAs, in the evolution of cancer cell drug resistance. MiRNAs have been characterized as major regulators of crucial genes implicated in the chemoresistance phenotype of gastric cancer cells. MiRNA-based therapy in the future may provide a new strategy to overcome drug resistance. This review summarizes the current knowledge on the role of miRNAs in regulating drug resistance in gastric cancer and their potential to develop targeted therapies and personalized treatment for managing drug resistant gastric cancers. [ABSTRACT FROM AUTHOR]

• Nanocurcumin supplementation increased Treg cells frequency significantly compared with baseline and placebo group. • Nanocurcumin supplementation increased FoxP3, TGF-β, IL‐10, miRNA-25, and miRNA-106b mRNA expression significantly compared to baseline and placebo group. • Nanocurcumin supplementation increased serum TGF-β and IL-10 significantly compared to baseline and placebo group. • Nanocurcumin supplementation decreased disease activity significantly compared to placebo group. Current research was designed to assess the effects of nanocurcumin supplementation on regulatory T (Treg) cells frequency and function in Behçet's disease (BD). In this randomized double-masked, placebo-controlled trial, 36 BD subjects were randomly put into two groups to take one 80 mg nanocurcumin capsule or placebo daily for 8 weeks. Before and after trial, disease activity, Treg cells frequency and expression of related immunologic parameters including forkhead box protein P3 (Foxp3) transcription factor messenger RNA (mRNA) and microRNAs (miRNAs) such as miRNA-25 and miRNA-106b as well as cytokines including transforming growth factor (TGF)-β and interleukin (IL)-10 were studied. Thirty-two patients (17 in the nanocurcumin and 15 in the placebo groups) completed the trial. Treg cells frequency increased significantly in the nanocurcumin group compared with baseline (P < 0.001) and placebo group (P < 0.001). Moreover, FoxP3, TGF-β, IL‐10, miRNA-25, and miRNA-106b mRNA expression levels increased considerably in the nanocurcumin group compared to baseline (P < 0.001) and placebo group (P < 0.001, P < 0.001, P = 0.025, P = 0.011, and P < 0.001, respectively). Significant increases in serum TGF-β and IL-10 were seen in nanocurcumin group compared with baseline (P < 0.001) and placebo group (P = 0.001 and P < 0.001, respectively). Significant decrease in disease activity was found in nanocurcumin group compared with placebo group (P = 0.044). Our study provided a promising view for desirable effects of nanocurcumin supplementation in improving immunological parameters and disease activity in BD. [ABSTRACT FROM AUTHOR]

Idiopathic membranous nephropathy (IMN) as a single organ autoimmune disease is a main cause of nephrotic syndrome in adults which is determined through autoantibodies to podocytes proteins. Th17/regulatory T (Treg) balance has emerged as a prominent factor in the regulation of autoimmunity. In this study, we evaluated the balance of Th17 and Treg cells, expression level of related master transcription factors, cytokines and microRNAs in mononuclear cells of peripheral blood of 30 patients with IMN and 30 healthy individuals before treatment. No significant variation was observed in Th17 cell frequency, retinoic acid receptor‐related orphan nuclear receptor γt (RORɣt), signal transducer and Activator of transcription 3(STAT3), IL-17, and IL-23, while IL-21, IL-4, and IL-10 had significant increase in mRNA expression and protein level of peripheral blood mononuclear cells in IMN cases. Reduction in the percentage of Treg cells was also accompanied with significantly decreased expression of Forkhead box P3(FOXP3) and Transforming growth factor beta (TGF-β) in IMN patients compared to the control group. Our study revealed that Th17 cells themselves might not be engaged in the pathogenesis of newly diagnosed patients with IMN; however, decreased T reg cells and increased ratio of Th17/Treg lymphocytes might display a role in the pathogenesis of IMN before treatment. [ABSTRACT FROM AUTHOR]