Bullous pemphigoid (BP) is an autoimmune blistering skin disease characterized by autoantibodies to hemidesmosomal proteins. The initiation and regulation of the autoimmune response are poorly understood. We analysed cell subsets with immunoregulatory functions in untreated BP patients. While the numbers of circulating NKT and NK cells were normal, gammadelta T cells were reduced in BP patients. gammadelta T cells were rarely detected in lesional skin, arguing against their sequestration in the skin. In most patients, clinical remission and reduction of autoantibody titres after immunosuppressive therapy was not accompanied by an increase of circulating gammadelta T cells. V gammadelta gene usage was not altered in BP patients and the gammadelta T cells of BP patients were functional as they proliferated in response to isopentenyl pyrophosphate. Our data provide a basis for further investigations on the role of gammadelta T cells in the immunopathogenesis of BP.