Immunological aspect in inflammatory bowel disease

Abstract

Inflammatory bowel disease (IBD) is a chronic inflammation in the alimentary tract due to improper immune response toward external and internal antigens. The disease consists of two entities: Ulcerative colitis and Crohn’s disease. The disease’s prevalence is increasing worldwide due to westernization and industrialization. Europe still holds the highest prevalence of IBD in the world. There are two peaks of disease incidence. The first is in the third decade of life and the second is in the fourth decade. Slight male predominance is observed in IBD. Internal and external risk factors play an important role in the occurrence of IBD including genetic, smoking, reduced fiber intake, less or absent breastfeeding, sedentary occupation, pollution exposure, and medications. The disease carries heavy economic burden and hampers patient’s quality of life. The immune concept of IBD was hypothesized in the 1950s since the symptoms resolved with the administration of steroid. Innate and adaptive immune systems are involved in the pathogenesis of IBD. Antigen-presenting cells are found hyperactive, intestinal barrier is disrupted, and autophagy activity is increased. Molecular mimicry occurs between foreign and self-antigen. The activity of T helper (Th)1, Th2, and Th17 is amplified while regulatory T-cell’s activity is suppressed. Pro-inflammatory cytokine production is elevated but anti-inflammatory cytokines are lowered. Finally, there is increased immunoglobulin G level in intestinal mucosa and imbalance of gut microorganism. All the above immune disturbances lead to chronic inflammation in IBD.