Marta Consuegra-Fernández, Marc Julià, Mario Martínez-Florensa, Fernando Aranda, Cristina Català, Noelia Armiger-Borràs, María-Teresa Arias, Francisca Santiago, Antonio Guilabert, Anna Esteve, Carlos Muñoz, Carlos Ferrándiz, José-Manuel Carrascosa, Edurne Pedrosa, Jorge Romaní, Mercè Alsina, José-Manuel Mascaró-Galy, Francisco Lozano
Psoriasis is a chronic inflammatory skin disease with a strong genetic background and is triggered by environmental factors. Available evidence supports CD6, a lymphocyte surface receptor mostly expressed by T cells, as a putative target in autoimmunity. Accordingly, a humanized anti-CD6 antibody has been assayed for the treatment of certain autoimmune disorders, including psoriasis. Here, we present novel evidence in mice and humans for a direct involvement of CD6 in psoriasis pathophysiology. First, an attenuated form of imiquimod-induced psoriasis-like skin inflammation was demonstrated in CD6-deficient mice, as deduced from lower epidermal thickness and local reduced production of pro-inflammatory cytokines, namely, interleukin-17A...
December 11, 2017: Cellular & Molecular Immunology