Bullous pemphigoid (BP) is an autoimmune blistering skin disease characterized by
large, tense blisters. Production of autoantibodies against the 180-kDa hemidesmosomal
protein of the basement membrane zone is regarded as the first event of the pathomechanism
[
[1]
]. Once the autoantibodies bind to the basement membrane, a cascade of inflammatory
events occurs, resulting in subsequent blister formation at the dermoepidermal junction.
During this process, cytokines and chemokines are considered to play crucial roles
in inflammatory cell recruitment, deposition and perpetuation [
[2]
]. Therefore, clarifying the serum and local levels of cytokines and chemokines may
help in understanding the immune dysregulation in the pathomechanism of BP.Keywords
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Article info
Publication history
Published online: July 12, 2010
Received:
March 18,
2008
Identification
Copyright
© 2008 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
