Abstract

During the last decades, a better understanding of the mechanisms sustaining the pathogenic process in inflammatory bowel diseases (IBD) has contributed to expand the therapeutic armamentarium for patients with these disorders. Alongside with traditional therapies, monoclonal antibodies against tumor necrosis factor-α, the interleukin (IL)-12/IL-23 p40 subunit and the α4β7 integrin, and tofacitinib, a small molecule inhibiting intracellular pathways downstream to cytokine receptors, have entered into the clinic. However, these drugs are not effective in all patients and some responders can lose response over time. Such a therapeutic failure is, at least in part, dependent on the fact that, in IBD, the tissue damage is driven by simultaneous activation of multiple and distinct immune-inflammatory signals and the detrimental mucosal immune response changes over time even in the same patient. Therefore, personalized approaches aimed at identifying which patient should be treated with a specific drug at a precise time point are worth pursuing. A such approach has the advantage to improve efficacy of the drug and limit adverse reactions, thereby improving quality of the life of the patients and reducing costs. In this review, we summarize all the available evidence about the possible role of precision medicine in IBD.

Highlights

  • Inflammatory bowel diseases (IBD) are chronic, disabling, immune-mediated disorders of the gastrointestinal tract encompassing two main clinical entities: Crohn’s disease (CD) and ulcerative colitis (UC) (Abraham and Cho, 2009)

  • We summarize all the available evidence about the possible role of precision medicine in IBD

  • The aetiology of IBD is unknown, it has been suggested that IBD-associated tissue damage process is induced by an exaggerated immune response against luminal antigens, which is favoured by genetic predisposition and environmental factors (Macdonald and Monteleone, 2005; Digby-Bell et al, 2020)

Read more

Summary

Introduction

Inflammatory bowel diseases (IBD) are chronic, disabling, immune-mediated disorders of the gastrointestinal tract encompassing two main clinical entities: Crohn’s disease (CD) and ulcerative colitis (UC) (Abraham and Cho, 2009). The possibility to collect mucosal samples from inflamed gut of IBD patients, the use of preclinical models of intestinal inflammation and the advent of sophisticated molecular technologies have led to a better understanding about the mechanisms by which the local immune response promotes gut damage. This progress has promoted the development of many pharmacological compounds, which can target key factors of the IBD-associated mucosal inflammation (Marafini et al, 2019).

Findings
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call