# Identification of T cell stress response state (TSTR) and key genes related to T cells in discoid lupus erythematosus

## TL;DR

This study identifies a unique T cell stress response state and key genes linked to T cells in discoid lupus erythematosus, offering potential biomarkers for diagnosis and understanding of the disease.

## Contribution

The study introduces a novel T cell stress response state (TSTR) and identifies key genes specific to discoid lupus erythematosus.

## Key findings

- TSTR cells are abundantly infiltrated in the dermis of discoid lupus erythematosus.
- CXCL13 and GNLY show distinct high expression in DLE, supporting their role as key biomarkers.
- Eight key genes are identified as central to T cell function and disease mechanisms in DLE.

## Abstract

The malignant transformation risk and high misdiagnosis rate of discoid lupus erythematosus (DLE) render it an urgent necessity to deeply explore its pathogenesis and biomarkers. This research, through the combined analysis of transcriptome data and single-cell sequencing data, commencing from the highly infiltrated T cells in DLE and the significant inflammation and cytokine correlation manifested by T cells, undertakes re-clustering analysis of T cells and identifies the stress response state T cells (TSTR) that are abundantly infiltrated in the dermis of DLE. Furthermore, by screening for the common genes among the differentially expressed genes in the transcriptome, the differentially expressed genes of T cells in single-cell sequencing, and the key module genes in WGCNA, CXCL13, GNLY, IFI6, IFI27, IFI44, IFI44L, MX1, and TIGIT are ultimately extracted as the key disease genes of DLE, and these genes are closely associated with the mechanism regulating T cell function. Specifically, through supplementary validation of gene expression using the psoriasis dataset, the distinctively high expression characteristics of CXCL13 and GNLY in DLE were revealed, thereby corroborating their central status as characteristic markers of DLE.

The online version contains supplementary material available at 10.1038/s41598-025-23088-7.