AI Article Synopsis
- Bullous pemphigoid (BP) is an autoimmune blistering disease mainly seen in older adults, significantly affecting their quality of life.
- The disease involves autoantibodies against specific proteins and displays characteristics of type 2 inflammation, including high levels of IgE and eosinophils, along with increased type 2 cytokines in skin lesions.
- This review highlights the pathophysiology of BP, the impact of biologics targeting type 2 immune mediators, and the potential for future targeted therapies to improve treatment options.
Article Abstract
Bullous pemphigoid (BP) is an autoimmune blistering disease that most often affects elderly individuals and has a significant negative impact on quality of life. The disease is characterized primarily by autoantibodies to hemidesmosomal proteins BP180 and/or BP230, and an inflammatory reaction with notable features of type 2 inflammation, including elevated serum IgE, increased numbers of eosinophils in lesions and peripheral blood, and elevated expression of type 2 cytokines and chemokines in skin lesions. In this review, we present what is known about BP pathophysiology, including the role of type 2 inflammation, and discuss how findings from studies of biologics targeting type 2 immune mediators have helped to clarify the biological mechanisms driving BP pathophysiology. Future studies of these targeted therapies and others in development will help to further elucidate the mechanisms underlying BP pathophysiology and potentially provide better treatment options for patients.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550233 | PMC |
| http://dx.doi.org/10.1007/s12325-024-02992-w | DOI Listing |
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