Journal
JOURNAL OF IMMUNOLOGY
Volume 169, Issue 7, Pages 3987-3992Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.7.3987
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Funding
- NIAID NIH HHS [R01 AI40768] Funding Source: Medline
- NIAMS NIH HHS [R01 AR32599, R01 AR032081, R01 AR040410, R37 AR32081] Funding Source: Medline
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Bullous pemphigoid (BP) is a subepidermal blistering disease associated with autoantibodies against two hemidesmosomal proteins, BP180 and BP230. Numerous inflammatory cells infiltrate the upper dermis in BP. We have previously shown by passive transfer studies that Abs to the ectodomain of murine BP180 are capable of triggering blisters in mice that closely mimic human BP. Experimental BP depends on complement activation and neutrophil infiltration. In the present study, we investigated the relative contribution of neutrophils, mast cells (MCs), macrophages (Mphi), and lymphocytes and their functional relationship in the immunopathogenesis of this disease model by using mice deficient in these cells. Wild-type, T cell-deficient, and T and B cell-deficient mice injected intradermally with pathogenic anti-murine BP180 IgG exhibited extensive subepidermal blisters. In contrast, mice deficient in neutrophils, MCs, and Mphi were resistant to experimental BP. MCs play a major role in neutrophil recruitment into the dermis. Furthermore, Mphi-mediated neutrophil infiltration depends on MC activation/degranulation.
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