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Bullous pemphigoid (BP) is an autoimmune blistering disorder that predominantly affects the elderly. Its pathogenesis involves the disruption of the basement membrane zone (BMZ), driven by pathogenic autoantibodies and a pronounced inflammatory response. Current first-line therapies, primarily based on glucocorticoids and immunosuppressants, are limited by substantial side effects and frequent disease recurrence. Regulatory T cells (Tregs) play a central role in maintaining immune homeostasis and peripheral tolerance, exerting control over effector immune cells through transcriptional regulation, surface markers, and diverse immunosuppressive mechanisms. Accumulating evidence indicates that numerical reduction and functional impairment of Tregs are critical to the breakdown of immune tolerance in BP. Treg dysfunction leads to the aberrant activation of Th2, Th17, and follicular helper T (Tfh) cells, which in turn promotes the production of anti-BP180/BP230 autoantibodies and disrupts the regulation of inflammatory cells such as neutrophils and eosinophils. These events collectively result in BMZ degradation and blister formation. Multiple factors, including age-related immunosenescence, genetic predisposition, pharmacological exposures, and environmental stimuli, can further compromise Treg function, thereby contributing to BP pathogenesis. A deeper understanding of Treg-driven mechanisms in BP provides a rational basis for developing targeted therapeutic strategies.
Wang et al. (Tue,) studied this question.