There has been a great deal of speculation (and experimentation) about the precise pathogenic role of bullous pemphigoid autoantibodies since their demonstration in 1964 by Beutner and Jordon1 and Jordon et al. in 1967,2 although there is considerable evidence that the autoantibodies are in fact responsible for the cutaneous lesions and are not just and epiphenomenon that has yet to be established beyond doubt. One of the reasons that there are still some questions rests with the fact that there is not a simple, reproducible animal model for production of the cutaneous lesions of BP in vivo, either by systemic passive transfer of the human autoantibodies or by immunization of animals with the BP antigen(s). Some studies have come very close to achieving this goal but have not succeeded entirely. The details of these studies, current thoughts on why these studies have not been successful as yet, and future directions for the definition of this problem are discussed in this chapter.
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