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Updated: Jul 15, 2026
07:46
In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
Published on: October 25, 2024
Dysregulation of T Helper 17 Cell Pathway In Vitiligo.
Vaibhav Venkatesh1, Deena Mendez2, Rajashekar T Srinivas3
1From the Department of Cell Biology and Molecular Genetics, Sri Devaraj Urs Academy of Higher Education and Research, Kolar, Karnataka, India.
Indian Journal of Dermatology
|July 13, 2026
Summary
The T helper 17 (Th17) cell pathway is overactive in vitiligo, contributing to autoimmune disease. This study investigated Th17 pathway components in vitiligo pathogenesis, revealing significant dysregulation.
Area of Science:
- Immunology
- Dermatology
- Genetics
Background:
- The T helper 17 (Th17) cell pathway plays a critical role in autoimmune responses and chronic inflammation.
- Vitiligo is an autoimmune disorder characterized by melanocyte destruction.
Purpose of the Study:
- To investigate the involvement of the Th17 cell pathway in the pathogenesis of vitiligo.
- To evaluate key components of the Th17 pathway, including modulatory cytokines, mediator gene expression, and effector cytokines.
Main Methods:
- A case-control study involving 30 vitiligo patients and 30 healthy controls.
- Plasma cytokine levels (IL6, IL23, IL10) measured using ELISA.
- Gene expression of STAT3 and RORC analyzed in peripheral blood mononuclear cells via real-time quantitative PCR.
Main Results:
- Vitiligo patients exhibited significantly higher plasma levels of IL6 (2.3-fold) and IL17A (1.6-fold) compared to controls.
- Elevated gene expression of STAT3 (2.27-fold) and RORC (3.8-fold) was observed in vitiligo patients.
- Plasma IL10 levels were significantly lower (2.5-fold) in vitiligo patients, while IL23 showed a non-significant increase.
Conclusions:
- The findings suggest a dysregulated and likely overactive Th17 cell pathway in vitiligo pathogenesis.
- These results highlight the Th17 pathway as a potential therapeutic target for vitiligo.
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