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Related Experiment Video

Updated: Feb 14, 2026

Transcriptome Analysis of Single Cells
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Bulk and Single-Cell Transcriptomics Reveal That SCO2 Drives Psoriasis via Activating CCR7+ Dendritic Cell.

Donger Chen1,2,3, Jing Yang1,2,3, Guoliang Zhou1,2,3

  • 1Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, China.

International Journal of Molecular Sciences
|February 13, 2026
PubMed
Summary

SCO2, a mitochondrial protein, drives psoriasis by altering keratinocyte metabolism and immune cell interactions. Targeting SCO2 may reduce inflammation and serve as a biomarker for metabolic changes in psoriatic lesions.

Keywords:
CCR7+ dendritic cellsMacrophage Migration Inhibitory Factor (MIF)SCO2lactatemachine learningpsoriasis

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Area of Science:

  • Immunology
  • Metabolic Biology
  • Dermatology

Background:

  • Psoriasis involves metabolic reprogramming, but lactate metabolism's role in keratinocyte immune dysfunction is unclear.
  • Mitochondrial dysfunction and altered metabolism are implicated in chronic inflammatory skin diseases like psoriasis.

Purpose of the Study:

  • To investigate the role of lactate metabolism in keratinocyte-mediated immune dysregulation in psoriasis.
  • To identify key genes and pathways linking keratinocyte metabolism to immune responses in psoriatic lesions.

Main Methods:

  • Integrated bulk and single-cell RNA sequencing of psoriatic lesions.
  • Immunofluorescence and metabolic assays to validate findings.
  • Analysis of keratinocyte-dendritic cell-T cell interactions.

Main Results:

  • SCO2 (mitochondrial protein) was identified as a key pathogenic gene upregulated in psoriatic lesions.
  • SCO2 overexpression in keratinocytes led to increased migration, pyruvate accumulation, and lactate retention.
  • SCO2-high keratinocytes promoted IL-23 production by CCR7+ dendritic cells via MIF signaling, driving T cell priming.

Conclusions:

  • SCO2 acts as an immunometabolic switch, connecting keratinocyte metabolism to adaptive immunity in psoriasis.
  • Targeting SCO2 could disrupt DC recruitment and IL-23-driven inflammation, offering a novel therapeutic strategy.
  • SCO2 may serve as a potential biomarker for metabolic dysregulation in psoriatic skin.