Abstract
Identification of key autoantigen(s) for any autoimmune disease can potentially provide rational design strategies for antigen-specific therapeutics which can down-regulate, or perhaps cure, the patient's autoaggressive immune response while having little or no effect on attendant ‘normal’ immunity. For rheumatoid arthritis (RA), autoantigen identification(s) lags behind other diseases such as multiple sclerosis, myasthenia gravis or even type I diabetes mellitus where most investigators agree that antigens like myelin basic protein, the acetylcholine receptor and glutamic acid decarboxylase are keys to the patient's loss of self-tolerance. However, recent advances in knowledge and understanding of the multiple and interacting signals involved in driving immune responses have provided strategies for selective inhibition of the autoaggressive response in RA. Clinical trials utilising these strategies are just beginning. Thus, a general but critical review of the two-signal model of immunity and the therapeutic technologies driven by these new basic immunology discoveries seems warranted.