EXACERBATION OF EXPERIMENTAL PSORIASIS SYMPTOMS IN DESMOGLEIN-4 DEFICIENT RATS IS MEDIATED BY INCREASED INFLAMMATION

MARÍA TAMARA MORENO SOSA; BELÉN SÁNCHEZ; FLAVIA NEIRA; ELISA O PIETROBON; GRACIELA ALMA JAHN; JUAN PABLO MACKERN OVERTI

Mar del Plata

Otro; LXVI Reunión Anual de la Sociedad Argentina de Inmunología; 2019

SAIC-SAI-SAFIS

Psoriasis is a chronic inflammatory skin disease, characterized by keratinocyte hyperproliferation, vasculature growth and leukocyte infiltration into the dermis and epidermis. Although it is known that desmogleins are proteins involved in cell adhesion mechanisms, their role in psoriasis has not been addressed. The aim of our work was to assess the impact of desmoglein-4 deficiency in the immunological response of the skin. To this end, OFA hr/hr rats, which are mutant for the desmoglein-4 gene and Sprague-Dawley (SD) wild type rats were used. Imiquimod (IMQ), which is an immune response modifier that acts via toll-like receptor 7 pathway, was administered to both rat strains in shaved skin for four days to generate psoriasis-like lesions. Skin biopsies from treated and untreated OFA and SD rats were weighed, minced, stained with PE-Cy5-anti CD45 and FITC-anti CD3 monoclonal antibodies and analyzed by flow cytometry. We observed that in both strains, CD45+, CD3+ cells in increased in IMQ-treated groups, but the rise was higher in OFA rats (p