CD8+ tissue-resident memory T cells induce oral lichen planus erosion via cytokine network
Abstract
CD8+ tissue-resident memory T (CD8+ Trm) cells play key roles in many immune-inflammation-related diseases. However, their characteristics in the pathological process of oral lichen planus (OLP) remains unclear. Therefore, we investigated the function of CD8+ Trm cells in the process of OLP. By using single-cell RNA sequencing profiling and spatial transcriptomics, we revealed that CD8+ Trm cells were predominantly located in the lamina propria adjacent to the basement membrane and were significantly increased in patients with erosive oral lichen planus (EOLP) compared to those with non-erosive OLP (NEOLP). Furthermore, these cells displayed enhanced cytokine production, including IFN-γ, TNF-α, and IL17, in patients with EOLP. And our clinical cohort of 1-year follow-up was also supported the above results in RNA level and protein level. In conclusion, our study provided a novel molecular mechanism for triggering OLP erosion by CD8+ Trm cells to secrete multiple cytokines, and new insight into the pathological development of OLP.
Data availability
The data of this study, including scRNA-seq data, ST data, and bulk RNA-seq data are available in the Gene Expression Omnibus (GEO) database, accession numbers GSE213345, GSE213346 and GSE211630.
Article and author information
Author details
Funding
National Natural Science Foundation of China (81730030)
- Qianming Chen
National Natural Science Foundation of China (81730030)
- Hao Xu
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: All individuals provided written informed consent and this study was supported by the Ethics Committee of West China Hospital of Stomatology Sichuan University [WCHSIRB-2019-167].
Copyright
© 2023, Qing et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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