This week, researchers report new findings that clarify the role of NOD2, a key molecular player in Crohn's Disease, in the cellular signaling pathways that control inflammatory responses. NOD2's clinical relevance is clear from the fact that it is encoded by a Crohn's Disease susceptibility gene.
Understanding NOD2 has posed a particularly intriguing challenge for researchers because it appears able to somehow both activate and inhibit inflammatory cytokine responses in the cell. The work is reported by Lewis Cantley and colleagues at Harvard Medical School.
Crohn's Disease is an autoimmune inflammatory disorder of the gastrointestinal tract and is histologically characterized by inflammation, epithelial ulceration, fissure formation, and stenosis of segments of the entire gastrointestinal tract. The disease leads to significant morbidity and is thought to result from an inappropriate immune response to bacteria that normally inhabit the gastrointestinal tract. Because Crohn's Disease is characterized by too much initial acute inflammation, and, subsequently, too little subsequent negative regulation of that inflammatory response, pro-inflammatory and anti-inflammatory pathways appear to be faulty.