The blisters are subepidermal, and there are eosinophilic leukocytes within the blister and within the dermis in the cell-rich variant. Eosinophilic spongiosis is seen in a few cases, and such cases may be confused with herpes gestationis if the age of the patient is not stated. Immunofluorescent studies reveal linear basement membrane C3 deposition, and in most cases, IgG deposition.

The pathogenesis of the blister formation is complex and not completely understood. Suffice it to say, autoantibodies are deposited in the hemidesmosome/lamina lucida area. The blister that is formed in the cell-poor variant is relatively 'clean' and  is primarily located in the zone of the anchoring filaments and lamina lucida. The proteloytic  enzymes released from the degranulation of eosinophilic leukocytes in the cell-rich variant cause more extensive damage not only in this area but on both sides of this zone. Once separation of the epidermis from the dermis has occurred in the cell-rich variant, however, the base of the blister appears to be relatively 'clean' by light microscopic examination.

	Scan power view of a subepidermal blister. Inflammatory cells are in the superficial dermis to the left of the blister.
	A high power view of the dermoepidermal junction to the left of the blister. Eosinophilic leukocytes have congregated at the dermoepidermal junction. Extensive vacuolar change is seen in this zone. This combination may be the earliest recognizable finding in an early lesion of bullous pemphigoid.
	A high power view of the right side of the blister. A solitary eosinophilic leukocyte remains in this area where there is separation of the epidermis from the dermis. There is edema and evidence of damage to the dermal papillae.
	A high power view of the left side of the blister. The fully formed blister has a relatively clean base. Eosinophilic leukocytes and  a few lymphocytes are within the blister.

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