Therapeutic prospects of microRNAs derived from mesenchymal stem cell extracellular vesicles in rheumatoid arthritis: a comprehensive overview.

Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by inflammatory joint damage. Recent studies have focused on the significance of microRNAs (miRNAs) in the pathogenesis of RA. Mesenchymal stem cells (MSCs) have emerged as a potential therapeutic option for RA based on their regenerative and immunomodulatory properties.

Harnessing the therapeutic potential of mesenchymal stem/stromal cell-derived extracellular vesicles as a novel cell-free therapy for animal models of multiple sclerosis.

Multiple sclerosis (MS) is a chronic, neuroinflammatory, and demyelinating disease of the central nervous system (CNS). Current treatments offer only limited relief from symptoms, and there is no cure. Mesenchymal stem/stromal cells (MSCs) have demonstrated therapeutic potential for MS.

Effect of Disease-Modifying Therapies on COVID-19 Vaccination Efficacy in Multiple Sclerosis Patients: A Comprehensive Review.

According to current knowledge, the etiopathogenesis of multiple sclerosis (MS) is complex, involving genetic background as well as several environmental factors that result in dysimmunity in the central nervous system (CNS). MS is an immune-mediated, inflammatory neurological disease affecting the CNS. As part of its attack on the axons of the CNS, MS witnesses varying degrees of myelin and axonal loss.

Gene expression of semaphorin-3A, semaphorin-7A, neuropilin-1, plexin-C1, and β1 integrin in treated-multiple sclerosis patients.

Objective: Recently, members of the semaphorin family have received major attention in various medical fields, especially autoimmunity. In this study, we selected semaphorin-3A (Sema3A), semaphorin-7A (Sema7A), and their receptors to determine the possible relationship between these molecules and multiple sclerosis (MS).

Method: We measured the gene expression of Sema3A, Sema7A, neuropilin-1 (NP-1), plexin-C1, and β1 integrin in the blood samples of relapsing-remitting multiple sclerosis (RRMS) patients, treated with high-dose interferon-β1a (IFN-β1a), low-dose IFN-β1a, IFN-β1b, and glatiramer acetate (GA) via quantitative real-time polymerase chain reaction (qRT-PCR) assay, and then, compared the results of treatment-naive patients with the healthy controls.

Assessment of CCL27 and IL-11 in Multiple Sclerosis Patients Treated with Interferon-β and Glatiramer Acetate.

Introduction: Multiple sclerosis (MS) is a neuroinflammatory autoimmune disease which involves the central nervous -system. Although the primary cause of MS is obscure, effects of some cytokine and chemokine patterns in both innate and adaptive immune systems have been described. -Objectives: Since limited studies have examined the role of interleukin (IL)-11 and chemokine CCL27 in MS, we aimed to identify changes in IL-11 and CCL27 gene expression and serum levels in relapsing-remitting MS (RRMS) patients, treated with interferon (IFN)-β and glatiramer acetate (GA).

Effects of interferon and glatiramer acetate on cytokine patterns in multiple sclerosis patients.

Multiple sclerosis (MS) is an unpredictable autoimmune disease, which causes neurodegeneration in the central nervous system. Since the main cause of MS remains obscure, in this study, we aimed to evaluate the serum levels of some cytokines, including interleukin-5 (IL-5), IL-8, IL-9, IL-17A, transforming growth factor-beta (TGF-β), and interferon-gamma (IFN-γ) in relapsing-remitting (RR)-MS patients, treated with IFN-β and glatiramer acetate (GA). Serum samples of RR-MS patients, treated with high-dose IFN-β1a, low-dose IFN-β1a, IFN-β1b, and GA, were assessed by ELISA assay and then compared with the results of treatment-naive patients and healthy controls.

Negative Regulation of Semaphorin-3A Expression in Peripheral Blood Mononuclear Cells Using MicroRNA-497-5p.

Background: Semaphorin-3A (Sema3A), as a secreted semaphorin, is an immune modulator molecule participating in the pathogenesis of autoimmune diseases. MicroRNAs (miRNAs) modulate the target-gene expression at the post-transcriptional level. It has been proposed that miRNAs may be crucial to the modulation of the function of semaphorins.

High Mobility Group box-1 (HMGB1) Protein As a Biomarker for Acute Cholecystitis.

Background: Acute cholecystitis is defined as gallbladder inflammation caused by obstruction of the cystic duct. The pro-inflammatory cytokine, high mobility group box-1 (HMGB1), has been found to hold critical roles in the pathogenesis of several different inflammatory diseases. This study aimed to determine the relationship between HMGB1 and acute cholecystitis, and examine the potential for this cytokine as a biomarker for clinical diagnosis.

Semaphorin-3A as An Immune Modulator Is Suppressed by MicroRNA-145-5p.

Objectives: Semaphorin-3A (SEMA3A) and its receptors are found on some immune cells and act as suppressors of immune cells over-activation. Considering the role of SEMA3A and its down-regulation in some autoimmune diseases, as well as our bioinformatics predictions, we assumed that miR-145-5p might affect SEMA3A expression. So, we aimed to determine the effect of miR-145-5p on SEMA3A gene expression level.

Decreased expression of Sema3A, an immune modulator, in blood sample of multiple sclerosis patients.

Semaphorin 3A (Sema3A) as an immune modulator could participate in the pathogenesis of autoimmune diseases. In the current study, we aimed to investigate Sema3A expression in peripheral blood mononuclear cells (PBMCs) and its serum level in relapsing-remitting multiple sclerosis (RRMS) patients. Fifteen newly determined and untreated RRMS patients were chosen and assessed in relapsing and remitting phases in compare with fifteen healthy individuals.