Abstract
Pemphigus is a group of autoimmune-mediated mucocutaneous blistering diseases characterized by acantholysis. Pemphigus has also been recognized in dogs and shares similar clinical characteristics and variants with human pemphigus. While relationships between human and canine pemphigus have been reported, gene expression patterns across species have not been described in the literature. We sought to perform gene expression analysis of lesional skin tissue from four dogs with various forms of pemphigus to examine gene expression during spontaneous disease in dogs. We found increased T and B cell signatures in canine pemphigus lesions compared to controls, as well as significant upregulation of CCL3, CCL4, CXCL10, and CXCL8 (IL8), among other genes. Similar chemokine/cytokine expression patterns and immune infiltrates have been reported in humans, suggesting that these genes play a role in spontaneous disease. Direct comparison of our dataset to previously published human pemphigus datasets revealed five conserved differentially expressed genes: CD19, WIF1, CXCL10, CD86, and S100A12. Our data expands our understanding of pemphigus and facilitates identification of biomarkers for prediction of disease prognosis and treatment response, which may be useful for future veterinary and human clinical trials.
Highlights
Pemphigus is a group of potentially life-threatening autoimmune blistering diseases characterized by acantholysis
We examined genes that were trending toward significance, as these might provide insights into additional genes driving pathogenesis of canine pemphigus, but were under-powered in our study of four cases (Figure 1C)
We found that genes enriched in localized human pemphigus foliaceous compared to pemphigus vulgaris, including CCL5 and CYP1B1 were captured in the canine differentially expressed genes (DEGs) when examined by two-tailed student’s t-tests (Figure 4B)
Summary
Pemphigus is a group of potentially life-threatening autoimmune blistering diseases characterized by acantholysis. In these diseases, IgG autoantibodies target intraepithelial adhesion molecules resulting in epidermal splitting and blister formation [1]. Pemphigus can be categorized into different subtypes including pemphigus vulgaris and pemphigus foliaceus, depending on the level of blistering in the epidermis. In the United States, pemphigus vulgaris is the most common subtype, primarily affecting women between 50 and 60 years of age [2, 6]. Pemphigus vulgaris is thought to result from autoantibody action against desmosomal components, primarily desmoglein (Dsg) 1 and Dsg 3, leading to acantholysis [7]
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