Transforming growth factor alpha promotes bullous pemphigoid pathogenesis by disrupting cell adhesion and inducing inflammation.

ABSTRACT: Bullous pemphigoid (BP) is a chronic autoimmune blistering disorder characterized by dermal-epidermal separation and immune cell infiltration. The mechanisms underlying epithelial barrier dysfunction in BP remain incompletely understood. Here, we identify transforming growth factor alpha (TGF-α) as a key regulator of BP pathogenesis through disruption of cellular junctions and induction of pro-inflammatory responses. Elevated TGF-α levels in BP lesions correlated with disease severity. Mechanistically, TGF-α downregulated BP180 expression, upregulated matrix metalloproteinases (MMPs), and enhanced chemokine secretion in keratinocytes via epidermal growth factor receptor (EGFR) activation and downstream phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling. Pharmacological inhibit

SUBMITTER: Wang S 

PROVIDER: S-EPMC12748357 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature