Welcome to the 47th Annual ESDR Meeting 2017
2017 EADV Guest Lecture
Lecture Title: Autoimmune bullous disorders – translational insights
Date: Saturday 30 September 2017, 11.35-12.05
Room: Europa Hall
Introduced by: Luca Borradori
The major focus of the Hertl lab is to characterize the immunological network leading to T cell dependent B cell activation, and eventually, autoantibody production in autoimmune bullous skin disorders and related diseases. Based on our improved understanding of the pathogenesis of pemphigus and the pemphigoids, novel targeted strategies, including immunoadsorption and rituximab, have been introduced into the therapeutic armamentarium of these potentially lethal and hard-to-treat-disorders. Our improved knowledge of various cutaneous autoantigens which may serve as targets in clinically unrelated inflammatory skin disorders has helped to understand the effector function of distinct T cell subsets involved in these inflammatory processes. Overall, also rare, pemphigus and pemphigoid, are increasingly recognized as model diseases of autoantibody-related autoimmunity in general.
Hertl, M., Eming, R., Veldman, C. (2006) T cell control in autoimmune bullous skin disorders. J. Clin. Invest. 116, 1159-66.
Thoma-Uszysnki, S., Uter, W., Schwietzke, S., Schuler, G., Borradori, L. and Hertl, M. (2006) Autoreactive T and B cells from bullous pemphigoid (BP) patients recognize identical regions of BP180 and BP230. J. Immunol. 176, 2015-23.
Eming R, Nagel A, Wolff-Franke S, Podstawa E, Debus D, Hertl M. (2008) Rituximab exerts a dual effect in pemphigus vulgaris. J. Invest. Dermatol. 128, 2850-8.
Rafei D, Müller R, Ishii N, Llamazares M, Hashimoto T, Hertl M, Eming R. (2011) IgG autoantibodies against desmocollin 3 in pemphigus sera induce loss of keratinocyte adhesion. Am. J. Pathol. 178, 718-23.
Eming R, Hennerici T, Bäcklund J, Feliciani C, Visconti KC, Willenborg S, Wohde J, Holmdahl R, Sonderstrup G, Hertl M. (2014) Pathogenic IgG antibodies against desmoglein 3 in pemphigus vulgaris are regulated by HLA-DRB1*04:02-restricted T cells. J. Immunol. 193, 4391-9.