Rheumatoid arthritis (RA) is a chronic inflammatory joint disease characterised by the formation of a hyperplastic pannus, as well as cartilage and bone damage. The pathogenesis of RA is complex and involves broad interactions between various cells present in the inflamed synovium, including fibroblast-like synoviocytes (FLSs), macrophages, and T cells, among others. Under inflammatory conditions, these cells are activated, further enhancing inflammatory responses and angiogenesis and promoting bone and cartilage degradation. Novel treatment methods for RA are greatly needed, and mesenchymal stromal cells (MSCs) have been suggested as a promising new regenerative and immunomodulatory treatment. In this paper, we present the interactions between MSCs and RA-FLSs, and macrophages and T cells, and summarise studies examining the use of MSCs in preclinical and clinical RA studies.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that leads to joint damage and physical dysfunction. The pathogenesis of RA is highly complex, involving genetic, epigenetic, immune, and metabolic factors, among others. Over the years, research has highlighted the importance of non-coding RNAs (ncRNAs) in regulating gene expression. Given their dysregulation in numerous conditions, ncRNAs are thought to play a role in pathological processes. In RA, aberrant levels of circulating long ncRNAs (lncRNAs) are commonly observed in peripheral blood, along with their dysregulated expression in peripheral blood mononuclear cells and synovial tissue. This review discusses the involvement of lncRNAs in inflammation and the aggressive characteristics of fibroblast-like synoviocytes, a key cellular population driving RA progression.

Extracellular vesicles (EVs) are membrane-bound structures released by cells that contain bioactive cargo such as cytokines or non-coding RNA. It is widely known that EVs influence the activity of other cells; they take part in the pathogenesis and compensatory mechanisms of multiple diseases. Frequently, EVs can share the properties of their source cells, thus allowing the use of EVs as non-cellular vectors or therapeutic agents. Importantly, these structures can express the ligand for the programmed cell death protein 1 (PD-L1). It binds to the PD-1 protein present on the immune cells, which suppresses the activity of T cells. The PD-1/PD-L1 axis is widely known in the field of oncology, as PD-L1 present on the surface of cancer cells inhibits cytotoxic activity of T cells, thus promoting cancer growth and treatment resistance. Immunotherapy prevents PD-1/PD-L1 binding and restores anticancer properties of the immune cells. By contrast, the above-mentioned binding is desired in the context of autoimmunity, where abnormal activity of immune cells is a hallmark element in the pathogenesis of these conditions. The aim of this review is to present and discuss the latest findings regarding the role of EVs-PD-L1 in cancer and autoimmunity.

Hepatitis C virus (HCV) is a hepatotropic virus that can be transmitted through unsafe medical procedures, such as injections, transfusions, and dental treatment. The infection may be self-limiting or manifest as a chronic form that induces liver fibrosis, cirrhosis, or progression into hepatocellular carcinoma (HCC). Epigenetic mechanisms are major regulators of gene expression. These mechanisms involve DNA methylation, histone modifications, and the activity of non-coding RNAs, which can enhance or suppress gene expression. Abnormal activity or the dysregulated expression of epigenetic molecules plays an important role in the pathogenesis of various pathological disorders, including inflammatory diseases and malignancies. In this review, we summarise the current evidence on epigenetic mechanisms involved in HCV infection and progression to HCC.

Melanoma is one of the most aggressive forms of cancer and the leading cause of death related to skin disease. Recent years have seen a significant increase in the number of cases of this type of cancer, underscoring the need to develop effective therapeutic strategies to control it. One of the most promising research directions in this field is anticancer immunotherapy, particularly the use of vaccines aimed at enhancing the body’s cellular immunity. Among the modern methods of this type, mRNA-based vaccines are prominent, gaining increasing importance as a potential tool in cancer therapy. Their main advantages include a relatively rapid and flexible production process, low production costs, and the ability to induce both humoral and cellular immune responses. Despite their numerous advantages, therapeutic mRNA vaccines also pose a number of scientific and technological challenges. These primarily concern the stability of mRNA molecules and their effective delivery to target cells. In this context, delivery systems such as lipid nanoparticles (LNPs) play a key role, protecting mRNA from degradation and facilitating its transport into the cell cytoplasm. Alternatively, systems based on biodegradable polymers are also being developed, which can provide controlled mRNA release and additional biocompatibility. However, before therapeutic mRNA vaccines become a routine component of cancer therapy, extensive clinical trials and a thorough understanding of their mechanisms of action are necessary. This paper provides an overview of the current knowledge regarding the structure and delivery methods of therapeutic mRNA vaccines, with a particular emphasis on their use in melanoma therapy. The results of clinical trials to date are also presented and the challenges associated with implementing this form of therapy in medical practice are discussed.

Non-coding RNA (ncRNA) encompasses a large family of molecules that are crucial regulators of gene expression. This family includes microRNA, piwi-interacting RNA, and long non-coding RNA (lncRNA); each class is associated with different mechanisms of action that influence gene expression. Based on the available evidence, these molecules have important roles in physiological and pathological processes. For example, ncRNAs are strongly implicated in oncogenesis by mediating the expression of tumour suppressors and oncogenes. This review comprehensively describes the latest findings regarding the roles of lncRNAs in the pathophysiology of melanoma. Key aspects of melanoma biology and various mechanisms regulated by lncRNAs are discussed. Furthermore, future areas exploring potential biomarkers and therapeutic targets are presented.