# Bulk and single-cell RNA-sequencing analyses revealed potential key genes and the role of CCL19/CCL21-CCR7 axis in hidradenitis suppurativa

**Authors:** Xiaodong Lai, Yan Yang, Haini Zhang, Chong Zhang, Meng Wang, Wanxin Chen, Baoxi Wang, Yan Yan

PMC · DOI: 10.1371/journal.pone.0322565 · PLOS One · 2025-06-02

## TL;DR

This study uses RNA sequencing to identify key genes and the role of the CCL19/CCL21-CCR7 axis in hidradenitis suppurativa, a chronic skin condition.

## Contribution

The study identifies novel hub genes and highlights the CCL19/CCL21-CCR7 axis as a potential therapeutic target in hidradenitis suppurativa.

## Key findings

- AKR1B10, IGFL2, WNK2, SLAMF7, and CCR7 were identified as potential hub genes and therapeutic targets for HS.
- CCL19 and CCL21 are produced by fibroblasts and dendritic cells, recruiting CCR7-associated immune cells like Treg cells.
- The CCL19/CCL21-CCR7 axis is suggested to play a crucial role in HS pathogenesis and disease progression.

## Abstract

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder, affecting the pilosebaceous unit in apocrine gland-rich areas, characterized by painful nodules, abscesses and draining tunnels. The underlying molecular and immunological mechanisms remain poorly understood. This study aimed to identify key gene expression patterns, hub genes, and analyze the potential role of the CCL19/CCL21-CCR7 axis in HS lesions and peripheral blood using bulk and single-cell RNA sequencing analyses. By employing an integrative approach that included three machine learning methods and subsequent validation on an independent dataset, we successfully identified AKR1B10, IGFL2, WNK2, SLAMF7, and CCR7 as potential hub genes and therapeutic targets for HS treatment. Furthermore, our study found that CCL19 and CCL21 may originate from various cells such as fibroblasts and dendritic cells, playing a crucial role in recruiting CCR7-associated immune cells, particularly Treg cells. The involvement of the CCL19/CCL21-CCR7 axis in HS pathogenesis suggests that other CCR7-expressing cells may also be recruited, contributing to disease progression. These findings significantly advance our understanding of HS pathogenesis offer promising avenues for future CCR7-targeted therapeutic interventions.

## Linked entities

- **Genes:** AKR1B10 (aldo-keto reductase family 1 member B10) [NCBI Gene 57016], IGFL2 (IGF like family member 2) [NCBI Gene 147920], WNK2 (WNK lysine deficient protein kinase 2) [NCBI Gene 65268], SLAMF7 (SLAM family member 7) [NCBI Gene 57823], CCR7 (C-C motif chemokine receptor 7) [NCBI Gene 1236], CCL19 (C-C motif chemokine ligand 19) [NCBI Gene 6363], CCL21 (C-C motif chemokine ligand 21) [NCBI Gene 6366]
- **Diseases:** hidradenitis suppurativa (MONDO:0006559)

## Full-text entities

- **Genes:** AKR1B10 (aldo-keto reductase family 1 member B10) [NCBI Gene 57016] {aka AKR1B11, AKR1B12, ALDRLn, ARL-1, ARL1, HIS}, IGFL2 (IGF like family member 2) [NCBI Gene 147920] {aka UNQ645, VPRI645}, CCL19 (C-C motif chemokine ligand 19) [NCBI Gene 6363] {aka CKb11, ELC, MIP-3b, MIP3B, SCYA19}, WNK2 (WNK lysine deficient protein kinase 2) [NCBI Gene 65268] {aka NY-CO-43, P/OKcl.13, PRKWNK2, SDCCAG43}, CCR7 (C-C motif chemokine receptor 7) [NCBI Gene 1236] {aka BLR2, CC-CKR-7, CCR-7, CD197, CDw197, CMKBR7}, CCL21 (C-C motif chemokine ligand 21) [NCBI Gene 6366] {aka 6Ckine, CKb9, ECL, SCYA21, SLC, TCA4}, SLAMF7 (SLAM family member 7) [NCBI Gene 57823] {aka 19A, CD319, CRACC, CS1}
- **Diseases:** inflammatory skin disorder (MESH:D012868), abscesses (MESH:D000038), HS (MESH:D017497)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12129208/full.md

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12129208/full.md

## References

46 references — full list in the complete paper: https://tomesphere.com/paper/PMC12129208/full.md

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Source: https://tomesphere.com/paper/PMC12129208