Pathogenesis of rheumatoid arthritis: one year in review 2026.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterised by joint destruction and extra-articular manifestations. It is well known that underlying the pathogenesis of the disease a complex interplay of genetic susceptibility, epigenetic modifications, and immune dysregulation takes place. Over the past year, basic and clinical research studies in the field of RA have been conducted, shedding further light on certain pathogenetic mechanisms not yet fully clarified. In particular, advances have been made in understanding the interaction between cells of the innate immune system, such as neutrophils and macrophages, and structural cells, such as fibroblast-like synoviocytes (FLS). Furthermore, due to recent findings obtained at cellular and molecular levels, it has been possible to better define the interactions between the innate and adaptive immune systems and to better explain how RA-specific antibodies can exert a regulatory effect on the innate immune system. Identifying new elements regulating the mechanisms underlying RA pathogenesis is crucial for designing new therapeutic strategies and utilising biomarkers useful for the diagnosis and managements of the disease.