Transfer of antibodies specific for mouse BP180 to other mice induces the formation of blisters similar to those seen in individuals with BP. However, Zhi Liu and colleagues found that these antibodies do not cause disease in mice lacking C4 (a crucial component of the classical complement pathway). In the absence of activation of the classical complement pathway, immune cells known as mast cells were not activated and neutrophils (another immune cell type) were not recruited to the skin. This study identifies a mechanism by which self-reactive antibodies can cause blister formation in mice, and might lead to new treatments for individuals with BP and other autoimmune blistering diseases, such as herpes gestationis -- which is a nonviral disease of pregnancy.
TITLE: Role of different pathways of the complement cascade in experimental bullous pemphigoid
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