Multidimensional RCD interactions and therapeutic interventions in SLE: The graphical abstract illustrates the convergence of various regulated cell death (RCD) pathways—apoptosis, necroptosis, pyroptosis, NETosis, autophagy, and ferroptosis—in the pathogenesis of systemic lupus erythematosus (SLE). It highlights key molecular targets within these pathways and their linkage to inflammatory and autoimmune responses.

Mitochondrial abnormalities are crucial in the progression of systemic lupus erythematosus (SLE), with key elements like mitochondrial DNA mutations, oxidative stress, and immune metabolic reprogramming leading to cellular death. These dysfunctions result in an array of SLE symptoms, pointing toward mitochondrial pathways as potential therapeutic targets for improved patient outcomes.

The expression levels of circEPSTI1 were significantly higher in childhood-onset systemic lupus erythematosus (SLE) patients compared with the healthy controls (HCs), juvenile dermatomyositis (JDM), and juvenile idiopathic arthritis (JIA) patients. CircEPSTI1 may represent a prospective biomarker of childhood-onset SLE.

Flow cytometric analysis of circulating lymphocytes was used to examine the differences in cell populations between SLE patients with or without nephritis and healthy blood donors.

Pathologically expanded CD4⁺PD-1⁺Foxp3⁻ T cells of patients with rheumatoid arthritis promoted the B-cell response in vitro.

Microarray datasets of rheumatoid arthritis (RA), osteoarthritis, and healthy control were downloaded from the Gene Expression Omnibus database. Venn diagram, principal component analysis, heat map, volcano map, gene set enrichment analysis, gene ontology, and Kyoto encyclopedia of genes and genomes were used to analyze the data. Synovial tissue was identified as the key research objects. Further by protein–protein interaction network analysis of the four synovial tissue datasets and validation with immunohistochemistry of patients with RA and collagen-induced arthritis mice models, we identified that SLAMF8 may be a key biomarker for RA.

Gingiva-derived mesenchymal stem cells Inhibit the proliferation and invasion of rheumatoid arthritis fibroblast-like synoviocytes via CD39/CD73 signaling pathway.

This review offers an introduction to the immunological functions of inflammasomes and elucidates their pivotal roles in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, inflammatory bowel disease, cryopyrin-associated periodic syndrome, psoriasis, Sjögren's syndrome, and ankylosing spondylitis. Additionally, this review highlights the importance of developing drugs targeting inflammasomes as promising therapeutic avenues.

Mast cells (MCs) and MC-derived tumor necrosis factor (TNF) are important in chronic inflammatory and autoimmune diseases and post-viral syndromes, having important mechanisms of action, and therapeutic potential. MC and MC-derived TNF activation are involved in conditions like COVID-19, and neuroinflammation, linking TNF to various pathological processes such as apoptosis, thrombosis, and mitochondrial dysfunction. Potential therapeutic benefits of treatments, like high-dose melatonin and low-dose naltrexone (LDN) for modulating MC activation and reducing TNF-induced inflammation, seem to be promising therapies. They could help prevent or treat immune-mediated illnesses. Future research is encouraged to explore holistic approaches for better treatment of chronic/auto-immune diseases and also consider social determinants of health.

The origin and history of autoimmunity and autoimmune diseases.

β2-Glycoprotein I is the major antigen of the autoimmune antiphospholipid syndrome (APS). It modulates hemostasis and the complement system, as well as playing an important role in vascular injury associated with APS.