A Brief Overview on Molecular Aspects of Models for Induction of RA for Target Validation

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, joint destruction, and systemic complications. Understanding its molecular and immunological mechanisms requires robust experimental models that replicate key features of the disease. Various in vivo models, including collagen-induced arthritis (CIA), collagen antibody-induced arthritis (CAIA), antigen-induced arthritis (AIA), SKG mouse model, and pristane- induced arthritis (PIA), provide insights into different aspects of RA pathogenesis. These models mimic processes such as autoantibody generation, T and B cell activation, cytokine-mediated inflammation, pannus formation, and cartilage/bone erosion. While each model has unique advantages such as CIA for adaptive immunity studies, CAIA for innate immune pathways, AIA for localized responses, SKG for genetic predisposition, and PIA for systemic chronicity none fully replicates human RA. Their combined application, along with molecular analyses, allows researchers to dissect immune mechanisms and evaluate novel therapeutic strategies, including biologics, small molecules, and targeted immunotherapies. Ethical considerations, guided by the 3Rs principle (replacement, reduction, refinement), remain integral to animal experimentation. Collectively, these models remain indispensable tools for translational rheumatology and preclinical drug development aimed at improving RA management.