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Related Experiment Video

Updated: Jul 26, 2025

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Psoriasis and Leprosy: An Arcane Relationship.

Gai Ge1, Jingzhe Shang2,3, Tian Gan1

  • 1Laboratory of Mycobacteria, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, People's Republic of China.

Journal of Inflammation Research
|June 20, 2023
PubMed
Summary
This summary is machine-generated.

Psoriasis patients with high IL-17 signaling markers may not develop leprosy. Conversely, elevated macrophage markers in leprosy patients suggest they are unlikely to have psoriasis, revealing distinct immune profiles.

Keywords:
CLEC4EIL-17ATh17 cellleprosymacrophagepsoriasis

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Area of Science:

  • Immunology
  • Dermatology
  • Genomics

Background:

  • Psoriasis (Ps) and leprosy are chronic inflammatory skin diseases with distinct immune system involvements.
  • The rare coexistence of psoriasis and leprosy suggests underlying molecular immune mechanisms that remain unclear.

Purpose of the Study:

  • To investigate the molecular immune mechanisms underlying the rare coexistence of psoriasis and leprosy.
  • To identify differentially expressed genes (DEGs) and key biological pathways distinguishing psoriasis from leprosy.

Main Methods:

  • RNA-sequencing (RNA-seq) was performed on skin biopsies from patients with psoriasis, lepromatous leprosy (L-lep), and tuberculoid leprosy (T-lep).
  • Bioinformatic analyses including Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), Gene Set Enrichment Analysis (GSEA), and protein-protein interaction (PPI) networks were employed.
  • Key DEGs were validated using quantitative real-time polymerase chain reaction (qRT-PCR).

Main Results:

  • The protein-protein interaction (PPI) network highlighted immune response, IL-17 signaling, and Toll-like receptor pathways differentiating psoriasis and leprosy.
  • Th17 markers (e.g., IL-17A, IL-19, IL-20, IL-36A, IL-36G, IL-22, LCN2) were upregulated in psoriasis compared to both L-lep and T-lep.
  • Macrophage biomarkers (CLEC4E, TREM2), SPP1, and dendritic cell (DC)-related markers (ITGAX) along with TNF-a showed lower expression in psoriasis and T-lep compared to L-lep.

Conclusions:

  • Elevated expression of IL-17 pathway markers and LCN2 in psoriasis patients may confer resistance to lepromatous leprosy.
  • High expression of CLEC4E, TREM2, and SPP1 in lepromatous leprosy patients suggests they are unlikely to concurrently have psoriasis.
  • Distinct molecular immune signatures differentiate psoriasis and leprosy, explaining their rare coexistence.