Peer-reviewed veterinary case report
Gene changes in skin of dogs with vesicular cutaneous lupus
By Keating, Treasa et al.·Published in Veterinary dermatology·2026·Coastal Veterinary Dermatology and Ear Clinic, United States·View original on PubMed →
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Original publication title: Microarray Gene Expression Analysis of Lesional Skin in Canine Vesicular Cutaneous Lupus Erythematosus (VCLE).
- Species:
- dog
Plain-English summary
A group of six dogs diagnosed with a rare autoimmune skin condition called vesicular cutaneous lupus erythematosus (VCLE) showed signs of skin lesions and inflammation. Researchers found that the affected skin had a significant increase in certain immune-related genes, indicating a strong immune response. This suggests that treatments targeting the immune system, particularly those involving interferon and JAK-STAT signaling pathways, could be effective for managing this condition. While the study focused on understanding the disease better, it highlights potential new treatment options for dogs suffering from VCLE.
People also search for: dog skin lesions autoimmune disease · vesicular cutaneous lupus erythematosus treatment · dog skin problems immune system
Abstract
BACKGROUND: Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. OBJECTIVE/HYPOTHESIS: To characterise gene expression changes in lesional skin from dogs with VCLE and identify immune pathways involved in disease pathogenesis. ANIMALS: Six client-owned dogs with clinically and histopathologically confirmed VCLE, and five healthy control dogs. MATERIALS AND METHODS: Formalin-fixed, paraffin-embedded lesional and control skin samples were analysed using the NanoString nCounter Canine Immuno-Oncology Panel, targeting 780 immune-related genes. Data were normalised using geNorm-selected housekeeping genes. Differential expression, cell type profiling and pathway enrichment analyses were also performed. RESULTS: Principal component analysis showed clear separation between VCLE and healthy control samples. A total of 491 differentially expressed genes were identified, including 439 upregulated and 52 downregulated genes (p-adj < 0.05). Lesional skin showed marked upregulation of interferon-stimulated genes (CXCL10, IDO1, ISG15, IFIT1), cytotoxic molecules (GZMB, PRF1, FASLG), pro-inflammatory chemokines (CXCL8, CCL3, CCL4) and S100 family markers (S100A12, S100A9, S100A8). Downregulated genes included DLA-DQB1, ERBB4, CCL27, GATA3 and RORC. Cell type profiling demonstrated enrichment of CD8T cells, cytotoxic T cells, natural killer cells, dendritic cells, macrophages and neutrophils. Pathway enrichment analysis identified activation of interferon signalling, Janus kinase signal transducer and activator of transcription (JAK-STAT) signalling, chemotaxis and cytotoxic immune pathways. CONCLUSIONS AND CLINICAL RELEVANCE: VCLE lesions feature a dominant interferon-stimulated gene signature, with downstream activation of JAK-STAT signalling and cytotoxic lymphocyte-mediated immune responses, suggesting that interferon and JAK-STAT signalling are potential therapeutic targets.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/42114565/