Case Series: Gene Expression Analysis in Canine Vogt-Koyanagi-Harada/Uveodermatologic Syndrome and Vitiligo Reveals Conserved Immunopathogenesis Pathways Between Dog and Human Autoimmune Pigmentary Disorders
December 2020
in “
Frontiers in Immunology
”
Vogt-Koyanagi-Harada syndrome vitiligo autoimmune pigmentary disorders T cell gene signatures IFNG TNF PRF1 IL15 CTSW CXCL10 CCL5 FOXP3 TBX21 IGFBP5 FOXO1 PECAM1 TGFB3 SFRP2 CXCL7 VKH T cells interferon gamma tumor necrosis factor perforin interleukin 15 cathepsin W C-X-C motif chemokine ligand 10 C-C motif chemokine ligand 5 forkhead box P3 T-box transcription factor TBX21 insulin-like growth factor-binding protein 5 forkhead box O1 platelet endothelial cell adhesion molecule transforming growth factor beta 3 secreted frizzled-related protein 2 C-X-C motif chemokine ligand 7
TLDR The immune processes causing VKH and vitiligo are similar in dogs and humans.
This study analyzed gene expression in canine Vogt-Koyanagi-Harada (VKH) syndrome and vitiligo, revealing conserved immunopathogenesis pathways between these disorders in dogs and humans. The research involved 2 VKH cases, 1 vitiligo case, and 5 healthy controls, highlighting a small sample size. Key findings included the upregulation of genes like TGFB3 and the involvement of T-cells and cytokines such as IFNG and TNF, suggesting enhanced T cell responses. The study indicated that dogs could serve as a model for human autoimmune pigmentary disorders, with potential therapeutic targets identified, such as the repurposing of JAK inhibitors. Further research was recommended to explore specific genes and pathways.
