Cartilage erosion in rheumatoid arthritis: studies in SCID mouse model

In the past few years there has been a growing interest in gene therapy to be used not only for the treatment of inherited, but also acquired, diseases. Although genetic factors have been frequently implicated in the pathogenesis of rheumatoid arthritis (RA) [1], and recent reports suggest mutations of tumor suppressor genes to play a role [2], RA is not caused by a specific genetic mutation. Much more likely it is an acquired disorder with a complex pathogenesis and yet unknown etiology. Gene therapy approaches in diseases such as RA differ from those in defined genetic disorders. Apart from the problem of how to correct a specific genetic abnormality, in RA another question appears to be crucial: that of which pathogenic pathway to modulate. Therefore, a suitable animal model for gene therapy approaches in RA should not only reflect relevant features of human disease but also permit one to analyze alterations in key disease processes as closely as possible to the conditions found in people.