Bench to Bedside in Autoimmunity: A Critical Review of Animal Models in Anti-Arthritic Drug Discovery

Rheumatoid arthritis is a long-term condition that affects the body systemically. It is marked by inflammation in the joints, invasion of immune cells damage to cartilage, destruction of bone and a slow decline in joint function. Development of rheumatoid arthritis involves interactions between the body’s immune system, including both innate and adaptive responses, animal models are still very important to know the complete pathophysiology of disease and possible treatments. Still no single animal model fully mirrors the immune features seen in human rheumatoid arthritis. Rheumatoid arthritis models include adjuvant-induced arthritis (AIA) collagen-induced arthritis (CIA) antigen-induced arthritis (AIAg) pristane-induced arthritis (PIA) collagen-antibody-induced arthritis (CAIA) K/BxN serum-transfer arthritis and genetically modified models. These models exhibit substantial diversity across their inductive triggers, kinetics of disease onset and chronicity, underlying immunopathogenic mechanisms, and patterns of histopathological damage. This review looks closely at the experimental models of rheumatoid arthritis. It covers how each one works, its strengths and weaknesses and how well it fits the goal of testing treatments for arthritis. Special attention is given to linking results with inflammatory markers oxidative stress indicators, tissue changes seen under a microscope and key molecular pathways, like NF-κB, MAPK, JAK/STAT and NLRP3. At the end a framework is suggested for choosing the model and validating results at the molecular level.