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Related Experiment Video

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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

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Published on: January 25, 2017

The interleukin-23 axis in intestinal inflammation.

Philip P Ahern¹, Ana Izcue, Kevin J Maloy

¹Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.

Immunological Reviews

|January 24, 2009

Summary

Interleukin-23 (IL-23) plays a dual role in intestinal immunity, influencing both inflammation and host protection. Targeting the IL-23 pathway offers potential for treating inflammatory bowel diseases (IBDs).

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Area of Science:

Immunology
Gastroenterology

Background:

Intestinal immune responses require strict regulation to balance protection and prevent pathology.
Interleukin-23 (IL-23) is a critical cytokine involved in maintaining intestinal homeostasis.
Dysregulation of IL-23 signaling is implicated in inflammatory bowel diseases (IBDs).

Purpose of the Study:

To explore the multifaceted roles of IL-23 in intestinal immunity.
To investigate the involvement of IL-23 in T-cell-mediated inflammatory pathways.
To identify IL-23 as a potential therapeutic target for IBD.

Main Methods:

Review of existing literature on IL-23 function in the intestine.
Analysis of IL-23's effects on T-helper 1 (Th1) and T-helper 17 (Th17) cells.
Examination of the association between IL-23 receptor polymorphisms and IBD susceptibility.

Main Results:

IL-23 orchestrates both T-cell-dependent and independent intestinal inflammation.
IL-23 restrains regulatory T-cell responses, promoting inflammation.
Polymorphisms in the IL-23 receptor are linked to IBD risk in humans.
IL-23 also contributes to beneficial host protective immunity and barrier function.

Conclusions:

IL-23 exhibits dual roles in intestinal immunity, promoting inflammation while also supporting host defense.
The IL-23 axis represents a conserved pathway crucial for intestinal homeostasis.
Targeting IL-23 and its downstream pathways may offer novel therapeutic strategies for IBD.