It has been proposed that autoantibody against the basement membrane zone (BMZ-Ab) is playing an impor tant role in the blister formation of bullous pemphigoid (BP). The reaction of the BMZ-Ab to the BMZ is supposed to induce chemotaxis in association with complement acti vation. The protease released from the infiltrate has been considered to cause blister at the dermal-epidermal junc tion [1], Recently, however, it has been reported by Nestor et al.[2] that the infiltrate in the bullous lesions of BP is composed mainly of helper/inducer T (TH) cells and macrophages. Previously. Hunyadi et al.[3] reported that autologous skin antigen stimulated lymphocytes in pa tients with BP. These reports suggest that the cell-mediated immune (CMI) reaction is also related to the mechanism of blister formation in BP.

In order to elucidate the CMI response in BP. we have attempted to find whether the lymphocytes infiltrating around the vesicle are stimulated immunologically. We have endeavored to determine the constitution of inflam matory infiltrates in the bullous lesion immunohistologically and we have also attempted to find whether the infil trated T cells are producing gamma-interferon (IFN-gamma) in the lesions. The bullous lesions of BP revealed that the inflammatory infiltrate was composed mainly of mononuclear cells around the vesicle. Langerhans’ cells were increased in number in the lesional epidermis of pa tients with BP. The inflammatory infiltrates include pre dominantly Leu3a+ cells showing TH cells. These cells were also HLA-DR+, which suggested activated THcells, and a number of the epidermal kératinocytes were also stained by HLA-DR MoAb. On the other hand. Leu 2a+ cells, which show suppressor/cy totoxic T cells, and Leu 12+ cells showing pan B cells were sparse. 11was of interest that some of the infiltrates were stained by anti-INF-gamma MoAb in the lesions. It has been suggested that they are