From the Guidelines
The immunopathogenesis of Inflammatory Bowel Disease (IBD) involves a complex interplay between genetic predisposition, environmental triggers, and immune system dysregulation, characterized by an imbalance between pro-inflammatory and anti-inflammatory cytokines, with the migration of lymphocytes from lymphoid tissues to the intestines promoting inflammation 1.
Key Factors
- The immune response is mediated by various cell types, including T-helper cells, which produce cytokines contributing to chronic inflammation and tissue damage.
- S1P signalling is involved in the pathogenesis of IBD, highlighting the importance of lymphocyte migration in the development of the disease 1.
- Treatment strategies aim to modulate this immune response, reducing inflammation and inducing clinical remission in patients with IBD.
Immunopathogenesis Details
- The imbalance between pro-inflammatory and anti-inflammatory cytokines plays a crucial role in the development of IBD, with tumour necrosis factor (TNF) inhibitors being a key treatment option 1.
- The emergence of biologic agents, such as integrin inhibitors and interleukin 12/23 inhibitors, has revolutionized the treatment of moderately to severely active IBD, allowing for steroid-free remission and reductions in hospitalizations and surgeries 1.
- Small molecule therapies, including Janus kinase (JAK) inhibitors, provide advantages such as oral administration and little to no risk of immunogenicity, making them a valuable treatment option for patients with IBD 1.
From the Research
Immunopathogenesis of Inflammatory Bowel Disease (IBD)
The immunopathogenesis of IBD is a complex process involving multiple factors, including:
- Abnormal gut microbiota
- Immune response dysregulation
- Environmental changes
- Gene variants 2, 3, 4, 5
- The role of the mucosal innate and adaptive immune system, including intestinal epithelial cells, innate lymphoid cells, and cells of the innate and adaptive immune system 6, 4
Key Players in IBD Immunopathogenesis
- T helper 17 (Th17) cells, which have been investigated for their effects on IBD, particularly in colitis 2
- Innate lymphoid cells (ILCs), a novel cell family that plays a role in the pathogenesis of IBD 2
- Genetic mutations that encode important aspects of innate immunity and mucosal homeostasis, which combine with environmental triggers to create inappropriate, sustained inflammatory responses 3
Mechanisms of IBD Immunopathogenesis
- The interplay between the intestinal epithelium, mucosal immune system, and commensal bacteria, which determines different outcomes based on environmental input 3
- The activation of innate immune response, which may be mediated by enhanced toll-like receptor activity, leading to the differentiation of naïve T-cells into effector T helper (Th) cells 4
- The role of antigen presenting cells in mediating the differentiation of naïve T-cells into effector T helper (Th) cells, including Th1, Th2, and Th17, which alter gut homeostasis and lead to IBD 4