The understanding of the pathophysiology of Crohn’s disease is currently undergoing a reassessment. The concept of this disease as a primary T cell disorder is being questioned, with a new emphasis on the role of innate immunity in initiating early events and in perpetuating the inflammatory state. Crohn’s disease has been proposed instead to result from impaired innate immunity, encompassing the mucosal barrier and cellular elements including neutrophils and macrophages. Recent advances in genetics, functional studies on innate immunity and therapeutic trials on patients with Crohn’s disease have lent support to this evolving hypothesis.
- GM-CSF, granulocyte macrophage colony-stimulating factor
- MDP, muramyl dipeptide
- NOD, nucleotide-binding oligomerisation domain
- TLR, toll-like receptor
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