Research Article Mediators of Mast Cells in Bullous Pemphigoid and Dermatitis Herpetiformis Agnieszka Zebrowska, 1 Malgorzata Wagrowska-Danilewicz, 2 Marian Danilewicz, 2 Olga Stasikowska-Kanicka, 2 Lilianna Kulczycka-Siennicka, 1 Anna Wozniacka, 1 and Elzbieta Waszczykowska 1 1 Department of Dermatology and Venereology, Medical University of Lodz, Plac Hallera 1, 90-497 Lodz, Poland 2 Laboratory of Nephropathology of Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland Correspondence should be addressed to Agnieszka Zebrowska; zebrowskaaga@wp.pl Received 29 June 2014; Revised 1 October 2014; Accepted 3 October 2014; Published 21 October 2014 Academic Editor: Magdalena Klink Copyright © 2014 Agnieszka Zebrowska et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Bullous pemphigoid (BP) and dermatitis herpetiformis (DH) are skin diseases associated with infammation. However, few fndings exist concerning the role of mast cells in autoimmune blistering disease. Skin biopsies were taken from 27 BP and 14 DH patients, as well as 20 healthy individuals. Immunohistochemistry was used to identify the localization and mast cell expression of TNF and MMP9 in skin lesions and perilesional skin. Te serum concentrations of TNF, MMP9, chymase, tryptase, PAF, and IL-4 were measured by immunoassay. TNF and MMP9 expression in the epidermis and in infammatory infuxed cells in the dermis was detected in skin biopsies from patients. Although these mediators were found to be expressed in the perilesional skin of all patients, the level was much lower than that in lesional skin. Increased serum PAF levels were observed in BP patients. Mast cells may play an essential role in activating infammation, which ultimately contributes to the tissue damage observed in BP and DH. Our fndings suggest that diferences in the pattern of cytokine expression directly contribute to variations in cellular infltration in DH and BP. 1. Introduction Dermatitis herpetiformis (DH) is one of the subepidermal autoimmune bullous diseases, which is characterized by skin and intestinal lesions. Skin lesions include polymorphic eruption accompanied by severe pruritus. Intestinal lesions are characterized by atrophy of intestinal villi resulting from immunological process [1]. Diagnosis of DH is established on the basis of a direct immunofuorescence test (DIF) revealing granular deposits of IgA in the papillae and the presence of circulating IgA antibodies directed against the endomysium and/or tissue and epidermal transglutaminase (tTG, eTG) [2, 3]. Skin lesions in DH are histologically characterized by neutrophilic infltrates leading to destruction of basement membrane zone (BMZ) proteins and anchoring fbers and blister formation [4–6]. Bullous pemphigoid (BP) is a blistering disease character- ized by infammatory infltrate in the dermis and the presence of IgG and C3 deposits along the BMZ and circulating IgG autoantibodies. Autoantibodies bound to autoantigens, the glycoproteins BPAG1 (230 kD) and BPAG2 (180 kD), local- ized in the basement membrane of the epidermis activate a series of immunological and enzymatic phenomena leading to the destruction of basement membrane components and the formation of blisters, as observed in DH [7, 8]. In the dermis, infammatory infltrates formed by eosin- ophils and neutrophils and bound in vivo deposits, can be observed along the basement membrane or at the top of papil- lae. Ultrastructural studies have also confrmed the presence of intensive infammatory infltrates at the dermoepidermal junction, as well as destruction of hemidesmosomes and components of the extracellular matrix [9]. Infltrate formation is preceded by early accumulation of leukocytes, depending on the activity of adhesion molecules. Te binding of autoantibodies leads to the activation of ker- atinocytes, which release cytokines, as well as the activation of Hindawi Publishing Corporation Mediators of Inflammation Volume 2014, Article ID 936545, 10 pages http://dx.doi.org/10.1155/2014/936545