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Related Experiment Video

Updated: Sep 12, 2025

Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro
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Testosterone Suppresses IL-17 Expression by Targeting RORγt Functions.

Akshay Binayke1,2, Rajdeep Dalal1,2, Charu Suri3

  • 1Immunology Core Laboratory, Translational Health Science and Technology Institute, Faridabad, India.

European Journal of Immunology
|August 5, 2025
PubMed
Summary

Testosterone suppresses inflammation by inhibiting T helper 17 (Th17) cell differentiation, offering new therapeutic targets for autoimmune diseases like psoriasis. This study reveals testosterone

Keywords:
IL‐17 | immune sex bias | immune sex dimorphism | psoriasis | testosterone | Th17

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Area of Science:

  • Immunology
  • Endocrinology
  • Dermatology

Background:

  • T helper 17 (Th17) cells are key drivers of autoimmune diseases.
  • Women exhibit higher susceptibility to autoimmune conditions, but underlying mechanisms are unclear.
  • Sex-based differences in immune responses, particularly involving Th17 cells, require further investigation.

Purpose of the Study:

  • To investigate the role of testosterone in modulating Interleukin-17 (IL-17) responses.
  • To explore the impact of testosterone on Th17 cell differentiation and its relevance to autoimmune pathogenesis.
  • To elucidate the molecular mechanisms by which testosterone influences Th17-mediated inflammation.

Main Methods:

  • Comparison of IL-17 levels and IL-17-expressing cells between male and female mice.
  • Evaluation of testosterone's effect on Th17 differentiation in vitro and in vivo.
  • Utilizing an imiquimod-induced psoriasis mouse model to assess therapeutic effects.
  • Molecular analysis to identify testosterone's interaction with key transcription factors like RORγt.

Main Results:

  • Testosterone supplementation ameliorated psoriasis severity in female mice.
  • Castration of male mice exacerbated psoriasis, indicating a protective role of endogenous testosterone.
  • Testosterone demonstrated inhibitory effects on both in vitro Th17 differentiation and in vivo IL-17 expression.
  • Testosterone was identified as an inverse agonist of RORγt (related orphan receptor gamma), a critical regulator of IL-17.

Conclusions:

  • Testosterone plays a significant role in limiting Th17-mediated tissue inflammation, particularly in psoriasis.
  • Findings provide mechanistic insights into sex differences in autoimmune disease susceptibility.
  • Testosterone derivatives targeting RORγt represent a potential therapeutic strategy for suppressing Th17-driven inflammatory conditions.