Abstract
Bullous pemphigoid (BP) is an autoimmune bullous disease exhibiting subepidermal blister formation. The deposition of autoantibodies and complement as well as inflammatory cell infiltrates including eosinophils, is observed in the lesions of BP, suggesting that cytokines play important roles in pathogenesis of this disease. Recent studies have extensively investigated cytokine expression in this disease using sera, blister fluid and biopsy specimens as samples. While BP is generally considered a Th2-mediated disease, cytokine/chemokine profiles in BP patients are too complex to conclude that it is ‘solely’ Th2 mediated. Further investigation of immune mediators is needed to elucidate the precise mechanism of the development of BP, as well as to develop therapeutic strategies targeting the inflammatory process of the disease.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
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