Abstract
Chronic arthritis is characterized by persistent joint inflammation and concomitant joint destruction. Animal models have been of great value in understanding potential pathogenetic pathways and studying therapeutic principles. The first models were based on T cell-driven pathways and taught us that arthritis can be induced by a variety of stimuli. This suggests that the involvement of a single (auto)antigen in rheumatoid arthritis is unlikely and suggests that the regulation of arthritis can best be approached via bystander suppression. Insight into the pivotal role of TNF alpha and IL-1 has emerged from studies employing a range of common and also novel transgenic models. Combination treatment with both TNF and IL-1 blockers is warranted to control both joint inflammation and joint destruction. Novel approaches with viral gene constructs of cytokines and cytokine inhibitors teach us that efficient gene therapy is a possibility for small joints.
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