Abstract

Background

Psoriasis, an inflammatory autoimmune disease, arises from intricate interactions between the immune system and epithelium. Recent reports have suggested new roles for gamma delta (γδ) T-cells in addition to immune surveillance, however, it remains to be determined whether the mechanisms identified in psoriasis murine models have a similar role in humans. The aim of the present study was to investigate the relationship between IL-17 A mRNA expression levels and γδ T-cell frequency in human psoriatic lesions, and to clarify the potential role of γδ T-cells in psoriasis pathogenesis.

Methods

The study involved 20 patients diagnosed with psoriasis and 16 control subjects. Expression of the IL-17 A gene was measured in formalin-fixed paraffin-embedded (FFPE) tissues by RT-PCR method. TCRγδ+ immunofluorescence staining was performed to measure the distribution of γδ T-cells in the same samples.

Results

In psoriatic lesion biopsies, TCRγδ+ T-cell percentage was found higher than the control samples. Additionally, psoriasis patients exhibited elevated levels of IL-17 A gene expression. In addition, this study showed a weak negative correlation between the proportion of γδ T-cells and IL-17 A mRNA expression in psoriatic skin samples.

Conclusion

A weak negative correlation between IL-17 A mRNA levels and γδ T-cell presence in human psoriasis lesions highlighting the novel effector functions of these cells in psoriasis pathogenesis.

Details

Title
IL-17 A expression negatively correlates with γδ T-Cell density in human psoriasis lesions: a novel implication for disease pathogenesis
Author
Sevgin, Kubra; Ozkanli, Seyma; Hekimoglu, Gulam; Yesilay, Gamze; Yucel, Nurullah; Canbaz, Halime Tuba; Seker, Muzaffer
Pages
1-8
Section
Research
Publication year
2025
Publication date
2025
Publisher
BioMed Central
e-ISSN
14712172
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3236996949
Copyright
© 2025. This work is licensed under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.