ArticleFrontiers in immunology2026
Could vector-derived cadherin mimicry contribute to pemphigus vulgaris? An immunogenetic and
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Introduction: Pemphigus vulgaris (PV) is a potentially life-threatening autoimmune blistering disease characterized by autoantibodies directed against the desmosomal cadherins desmoglein 3 (DSG3) and desmoglein 1 (DSG1), which are essential for keratinocyte adhesion. While the pathogenic role of these autoantibodies is well established, the upstream events leading to loss of immune tolerance against desmogleins remain incompletely understood. Genetic susceptibility conferred by HLA class II alleles and environmental exposures are thought to interact during disease initiation. In this study, we investigated Methods: Results: HLA-DRB1*04:02 and HLA-DRB1*14:01 alleles were significantly enriched in PV patients compared with controls, and the heterozygous HLA-DRB1*04:02/14:01 genotype was overrepresented in the patient cohort. Structural and energetic analyses indicated that selected vector-derived cadherin-like peptides can adopt stable conformations when bound to these HLA variants and display conformational features compatible with DSG3 ectodomain-derived peptides. Discussion: These findings highlight strong immunogenetic associations in PV and introduce a structurally and immunogenetically informed, hypothesis-generating Vector-derived Cadherin Mimicry (VCM) framework. By integrating genetic association data with computational modeling, this conceptual model suggests that repeated exposure to vector-derived cadherin-like proteins may represent a plausible environmental component contributing to PV susceptibility in genetically predisposed individuals. Experimental validation will be required to further evaluate this framework and its relevance to PV pathogenesis.
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