The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases

Figure 4

The paranoid overstimulated intestinal epithelial cell in Crohn’s disease. The deficiency in NOD2 inhibits an anti-inflammatory mechanism that impedes TLR2 from continual signaling if in contact with its bacterial wall ligands. The loss of this compensatory anti-inflammatory mechanism generates uncontrolled inflammation based on a threat that is not real, because the commensal flora does not harm.