# Reduced EZH2 Expression in Circulating CD8‐Positive T Cells and Monocytes in Psoriasis

**Authors:** Toyoki Yamamoto, Rino Toyoshima, Lixin Li, Asumi Koyama, Shinichi Sato, Sayaka Shibata

PMC · DOI: 10.1111/exd.70207 · Experimental Dermatology · 2026-01-10

## TL;DR

This study finds reduced EZH2 levels in immune cells of psoriasis patients, suggesting a role in disease progression and inflammation.

## Contribution

The study reveals a novel link between reduced EZH2 expression in immune cells and psoriasis pathogenesis.

## Key findings

- EZH2 expression is significantly reduced in CD8+ T cells and monocytes from psoriasis patients.
- Lower EZH2 levels in CD8+ T cells correlate with higher disease severity in psoriasis.
- EZH2 inhibition reduces IL-17A expression, indicating a role in inflammatory responses.

## Abstract

Enhancer of Zeste Homologue 2 (EZH2) is an epigenetic regulator involved in immune cell differentiation and function; however, its role in psoriasis remains unknown. This study aimed to evaluate EZH2 expression in peripheral blood mononuclear cells from patients with psoriasis and explore its potential functional relevance to disease pathogenesis. Peripheral blood samples were obtained from 40 psoriasis patients and 18 healthy controls, and EZH2 expression in T cell and monocyte subsets was analysed by flow cytometry. EZH2 expression was significantly reduced in circulating CD8+ naïve and memory T cells, as well as in monocyte subsets from psoriasis patients compared to healthy controls. EZH2 levels in CD8+ naïve T cells showed a significant inverse correlation with disease severity scores. Functional analyses revealed that pharmacological EZH2 inhibition suppressed IL‐17A expression in peripheral blood mononuclear cells under IL‐23/IL‐1β stimulation. In addition, immunofluorescence staining identified EZH2‐positive T cells and monocytes within psoriatic skin lesions. Collectively, these findings suggest that EZH2 may be involved in the regulation of type 3 inflammatory responses and may therefore represent an epigenetic regulator contributing to psoriasis pathogenesis.

## Linked entities

- **Genes:** EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) [NCBI Gene 2146]
- **Proteins:** IL17A (interleukin 17A), IL37 (interleukin 37), IL1B (interleukin 1 beta)
- **Diseases:** psoriasis (MONDO:0005083)

## Full-text entities

- **Genes:** EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) [NCBI Gene 2146] {aka ENX-1, ENX1, EZH2b, KMT6, KMT6A, WVS}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** Psoriasis (MESH:D011565), type 3 inflammatory (MESH:C565764), psoriatic skin lesions (MESH:D012871)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12790368/full.md

## References

33 references — full list in the complete paper: https://tomesphere.com/paper/PMC12790368/full.md

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Source: https://tomesphere.com/paper/PMC12790368