Background: Despite ongoing intensive research using sophisticated new
molecular tools and methods, the pathogenesis of autoimmune diseases
such as rheumatoid arthritis (RA) is still not completely understood.
Hypothesis: In this paper the two favorite hypotheses of the pathogene
sis of rheumatoid arthritis currently discussed are introduced and com
pared. Hypothesis 1 is focussing on the central rule of the T cells an
d T cell dependent phenomena in the pathogenetic scenario of RA. In co
ntrast, hypothesis 2 stresses the role of altered synovial fibroblasts
and their specific features critical for the destruction of inflamed
joints. Both hypotheses are thoroughly discussed and suggestions for f
urther research activities are made. Conclusion: Insights in the patho
genesis of RA provide options to develop new therapeutic strategies ai
med at the inhibition of pathogenetic relevant processes.