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Related Experiment Video

Updated: Jun 25, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

Interleukin-23/Th17 pathways and inflammatory bowel disease.

Clara Abraham¹, Judy Cho

¹Department of Medicine, Digestive Diseases, Yale University, New Haven, Connecticut 06520, USA. clara.abraham@yale.edu

Inflammatory Bowel Diseases

|March 3, 2009

Summary

The IL-23/Th17 pathway is crucial in chronic inflammatory diseases like inflammatory bowel disease (IBD). Its dysregulation impacts immune homeostasis, contributing to intestinal inflammation and autoimmunity.

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Area of Science:

Immunology
Gastroenterology

Background:

The IL-23/Th17 pathway is implicated in chronic inflammatory diseases.
Genetic associations in IBD patients highlight the pathway's role in intestinal immune homeostasis.

Purpose of the Study:

To elucidate the role of the IL-23/Th17 pathway in intestinal inflammation and immune homeostasis.

Main Methods:

Review of genetic associations in IBD patients.
Analysis of IL-23's function in CD4+ Th17 cells and other cell types.
Examination of the balance between effector T cells and regulatory T cells.

Main Results:

IL-23 influences CD4+ Th17 cells (IL-17 secretion, RORγt expression).
Dysregulation of Th17/Treg balance contributes to inflammation and autoimmunity.
The pathway is involved in microbial defense and intestinal inflammation.

Conclusions:

Proper regulation of the IL-23/Th17 pathway is essential for intestinal immune homeostasis.
Pathway dysregulation is a key factor in inflammatory bowel disease pathogenesis.