U lcerative Colitis and Crohn's disease, collectively termed inflammatory bowel disease (IBD), are chronic inflammatory diseases of the gastrointestinal tract. The diseases are characterized by bloody diarrhea, abdominal pain, weight loss, fatigue, and increased risk of gastrointestinal malignancy. Understanding the molecular pathogenesis of IBD is critical toward developing new therapies. IBD appears to result from an inappropriate response to normal gastrointestinal flora. The normal mucosal immune system represents a balance between aggressive cells and regulatory cells that can suppress the activity of the former. This balance can be disturbed by either an enhanced effector cell response of the innate or adaptive immune system, or a deficiency of a regulatory mechanism. We will explore the role of innate immunity and apoptosis and how defects can lead to the imbalance seen in IBD.
No takes yet. Share an insight, caveat, or question.
Lichtenberger et al. (2004) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: