Possible pathogenic mechanisms in rheumatoid arthritis (RA) patients and murine experimental models included [6], [16] (1) NOD2 functions to induce proinflammatory effects in the inflamed joint, whereas NOD1 has mainly an inhibitory role, exemplified by the inhibition of cytokine production and decrease in cell influx in a model of streptococcal cell wall (SCW)-induced arthritis; (2) NOD2 act synergistically with TLR in the production of proinflammatory and destructive mediators in RA patients. This evidence concerns the gene NOD2 and arthritic joint disease.