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Related Experiment Video

Updated: May 31, 2026

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse

In Vitro Differentiation of Naive CD4⁺ T Cells into Pathogenic Th17 Cells in Mouse

Published on: October 25, 2024

Nuclear receptors: TH17 cell control from within.

L Klotz¹, P Knolle

¹University of Muenster, Clinic for Neurology-Inflammatory Disorders of the Nervous System and Neurooncology, Muenster, Germany. luisa.klotz@ukmuenster.de

|July 13, 2011

Summary

Nuclear receptors regulate T helper 17 (T(H)17) cell differentiation, a key factor in autoimmune diseases. This review details how these receptors control T(H)17 development and immunity.

Area of Science:

Immunology
Molecular Biology
Cell Biology

Background:

T helper 17 (T(H)17) cells are implicated in autoimmune disease pathogenesis.
Mechanisms of T(H)17 cell development are not fully understood, particularly T cell-intrinsic factors.
Nuclear receptors, including the master regulator RORγt, play critical roles in T(H)17 differentiation.

Purpose of the Study:

To review current knowledge on the regulatory roles of nuclear receptors in T(H)17 cell differentiation.
To highlight the significance of nuclear receptors beyond RORγt in T(H)17 biology.
To explore how nuclear receptors influence the balance between T(H)17-mediated autoimmunity and protection.

Main Methods:

Literature review of studies on T(H)17 cell differentiation and nuclear receptor function.

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Analysis of molecular mechanisms governing T(H)17 development.

Synthesis of findings on the dual role of nuclear receptors in promoting and suppressing T(H)17-related conditions.

Main Results:

RORγt is essential for T(H)17 cell differentiation.
Other nuclear receptors also modulate T(H)17 development.
Nuclear receptors influence the susceptibility and protection against T(H)17-mediated autoimmune diseases.

Conclusions:

Nuclear receptors are critical regulators of T(H)17 cell differentiation.
Targeting nuclear receptors may offer therapeutic strategies for autoimmune diseases.
Further research into nuclear receptor function in T(H)17 cells is warranted.