Abstract： Bullous pemphigoid (BP) is a common autoimmune blistering skin disease. Studies on its immunologic pathogenesis have been always carried out at home and abroad. IgG autoantibodies, which are the predominant type of pathogenic autoantibodies, can bind to multiple BP180 epitopes, result in the fixation and activation of complement, degranulation of resident mast cells, activation of infiltrating inflammatory cells and release of proteinases followed by the loss of cell-matrix adhesion structure at the dermal-epidermal junction, and finally cause the formation of subepidermal blisters. Although studies have shown that both humoral and cellular immunity are involved, little is known about the resource of autoantibodies, probalble existent autoantigens, and the roles of eosinophils in the pathogenesis of BP.