Mesenchymal stem cells (MSCs) have great potential to differentiate into various types of cells, including but not limited to, adipocytes, chondrocytes and osteoblasts. In addition to their progenitor characteristics, MSCs hold unique immunomodulatory properties that provide new opportunities in the treatment of autoimmune diseases, and can serve as a promising tool in stem cell-based therapy. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder that deteriorates quality and function of the synovium membrane, resulting in chronic inflammation, pain and progressive cartilage and bone destruction. The mechanism of RA pathogenesis is associated with dysregulation of innate and adaptive immunity. Current conventional treatments by steroid drugs, antirheumatic drugs and biological agents are being applied in clinical practice. However, long-term use of these drugs causes side effects, and some RA patients may acquire resistance to these drugs. In this regard, recently investigated MSC-based therapy is considered as a promising approach in RA treatment. In this study, we review conventional and modern treatment approaches, such as MSC-based therapy through the understanding of the link between MSCs and the innate and adaptive immune systems. Moreover, we discuss recent achievements in preclinical and clinical studies as well as various strategies for the enhancement of MSC immunoregulatory properties.

Introduction: Behçet’s disease (BD) as systemic vasculitis of unknown etiology is associated with HLA-B*51 in European and Asian populations. HLA-A*26 was claimed as an additional BD susceptibility marker in Japanese and Greek patients. This study was performed to test for HLA associations in HLA-B*51 negative German and Turkish BD populations. Methods: In total, 65 German and 46 Turkish patients lacking HLA-B*51 were analyzed in comparison to healthy HLA-B*51 negative Germans (n = 1500) and Turks (n = 130). HLA-A/B genotypes were determined by SSOP. P-values with correction for multiple testing (p_c), χ2- test and odds ratio (OR) were used for statistical evaluation. Results: HLA-A*26 was significantly more frequent in HLA-B*51⁻ German patients [p_c = 0.0076, OR = 3.23, 95% CI 1.63 to 6.39] than in respective controls. HLA-A*26 was also elevated in a smaller group of Turkish patients versus the controls. Significant association of HLA-Bw4 with isoleucine at amino-acid position 80 (HLA-Bw4-80I) was found in the HLA-B*51⁻ German cohort of BD patients [p_c = 0.0042, OR = 2.35, 95% CI 1.41 to 3.93) and in the Turkish patients in comparison to the respective controls [p = 0.025, OR = 2.17, 95% CI 1.09 to 4.31]. On the contrary, HLA-Bw4-80 T was reduced in both HLA-B*51⁻ BD patient cohorts. Conclusions: The study shows a significant association of HLA-Bw4-80I present on HLA-B*51 as well as on other B-locus molecules with BD. This indicates that distinctive Bw4 epitopes on HLA-B locus molecules could play a role in BD pathogenesis. The study also indicates an association with HLA-A*26 in German and Turkish BD patients as a genetic risk factor independent of HLA-B*51.

The review is devoted to the relationship between the pathogenetic mechanisms of coronavirus infection (COVID-19) and immunoinflammatory rheumatic diseases (IRD). The current knowledge on the pathogenesis of COVID-19 is summarized, including the mechanisms of coagulopathy, hyperproduction of pro-inflammatory cytokines, and antiphospholipid antibodies that are common with IRD. The presence and clinical significance of detection of various autoantibodies in COVID-19, which probably play a pathogenetic role in immune dysregulation, were analyzed. Based on the data of recent studies, risk factors and features of the severe course of infection in patients with IRD are considered.

Background and Objectives: The coronavirus disease of 2019 (COVID-19) pandemic has posed a serious threat to humanity and is considered a global health emergency. Antimalarial drugs (ADs) have been used in the treatment of immuno-inflammatory arthritis (IIA) and coronavirus infection (COVID-19). The aim of this review is to analyze the current knowledge about the immunomodulatory and antiviral mechanisms of action, characteristics of use, and side effects of antimalarial drugs. Material and Methods: A literature search was carried out using PubMed, MEDLINE, SCOPUS, and Google Scholar databases. The inclusion criteria were the results of randomized and cohort studies, meta-analyses, systematic reviews, and original full-text manuscripts in the English language containing statistically confirmed conclusions. The exclusion criteria were summary reports, newspaper articles, and personal messages. Qualitative methods were used for theoretical knowledge on antimalarial drug usage in AIRDs and SARS-CoV-2 such as a summarization of the literature and a comparison of the treatment methods. Results: The ADs were considered a “candidate” for the therapy of a new coronavirus infection due to mechanisms of antiviral activity, such as interactions with endocytic pathways, the prevention of glycosylation of the ACE2 receptors, blocking sialic acid receptors, and reducing the manifestations of cytokine storms. The majority of clinical trials suggest no role of antimalarial drugs in COVID-19 treatment or prevention. These circumstances do not allow for their use in the treatment and prevention of COVID-19. Conclusions: The mechanisms of hydroxychloroquine are related to potential cardiotoxic manifestations and demonstrate potential adverse effects when used for COVID-19. Furthermore, the need for high doses in the treatment of viral infections increases the likelihood of gastrointestinal side effects, the prolongation of QT, and retinopathy. Large randomized clinical trials (RCTs) have refuted the fact that there is a positive effect on the course and results of COVID-19.

Introduction: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has had an unprecedented impact on people around the world, particularly those who were suffering from autoimmune rheumatic diseases (AIRDs). The world community acknowledges the significance of COVID-19...

Background: Viral infections, including coronavirus disease 2019 (COVID-19), in patients with autoimmune rheumatic diseases (AIRDs) tend to present more severe disease. This study aims to investigate the clinical characteristics and risk factors for severe infection in rheumatologic patients. Methods: We included patients with a diagnosis of AIRD and COVID-19 infection between January 2022 and July 2023. Patients with AIRDs infected with SARS-CoV-2 were matched with control patients of the general population according to age (±5 years) and sex in a 1:1 ratio. Confirmed infection was defined if a patient had a positive polymerase chain reaction (PCR) test. The severity was divided into mild, moderate, severe, and critical according to the guidelines of the United States National Institutes of Health (NIH). Results: A total of 140 individuals (37 males, 103 females; mean age 56.1 ± 11.3 years) with rheumatic disease diagnosed with COVID-19 infection were enrolled in the study. AIRDs included rheumatoid arthritis (RA) (n = 63, 45%), ankylosing spondylitis (AS) (n = 35, 25%), systemic lupus erythematosus (SLE) (n = 26, 8.6%), and systemic sclerosis (SSc) (n = 16, 11.4%). The AIRDs group had more SARS-CoV-2-related dyspnea (38.6%), arthralgia (45.7%), and depression (27.1%) than the control group (p = 0.004). The rate of lung infiltration on radiographic examination was higher in 58 (41.4%, p = 0.005) patients with rheumatic diseases than in those without them. Severe SARS-CoV-2 infection was more common in the AIRDs group than in the control group (22% vs. 12%; p = 0.043). Conclusions: Patients with AIRDs experienced more symptoms of arthralgia, depression, and dyspnea. There was a trend towards an increased severity of the disease in patients with AIRDs. Patients with arterial hypertension, diabetes, chronic lung, and kidney disease, treated with corticosteroids, had a longer duration, and high activity of autoimmune disease had an increased risk of severe COVID-19.