Exacerbation of experimental psoriasis symptoms in desmoglein-4 deficient rats is mediated by increased inflammation.

MORENO-SOSA MT; SANCHEZ MB; NEIRA FJ; PIETROBON EO; JAHN GA; MACKERN OBERTI JP

Mar del Plata

Congreso; LXIII Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica; 2018

Sociedad Argentina de Investigación Clínica

Psoriasis is a chronic inflammatory skin disease, characterized bykeratinocyte hyperproliferation, vasculature growth and leukocyteinfiltration into the dermis and epidermis. Although it is known thatdesmogleins are proteins involved in cell adhesion mechanisms,their role in psoriasis has not been addressed. The aim of our workwas to assess the impact of desmoglein-4 deficiency in the immunologicalresponse of the skin. To this end, OFA hr/hr rats, whichare mutant for the desmoglein-4 gene and Sprague-Dawley (SD)wild type rats were used. Imiquimod (IMQ), which is an immune responsemodifier that acts via toll-like receptor 7 pathway, was administeredto both rat strains in shaved skin for four days to generatepsoriasis-like lesions. Skin biopsies from treated and untreated OFAand SD rats were weighed, minced, stained with PE-Cy5-anti CD45and FITC-anti CD3 monoclonal antibodies and analyzed by flow cytometry.We observed that in both strains, CD45+, CD3+ cells inincreased in IMQ-treated groups, but the rise was higher in OFA rats(p