Desmoglein-4 deficiency increases resident CD3+ T cell subset in a rat psoriasis model.

MORENO-SOSA MT; PIETROBON EO; INNOCENTI-BADANO AC; SOAJE M; VALDEZ SR; SANCHEZ MB; YUDICA-SEDANO F; NEIRA FJ; PENNACCHIO GE; JAHN GA; MACKERN OBERTI JP

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

Reunión Conjunta de Sociedades de Biociencias

It is known that desmogleins are involved in cell adhesion mechanisms and are crucial in keeping structural integrity of different tissues, including skin. They also play important roles in differentiation, cell activation and migration. Keratinocytes (KC) produce several inflammatory factors that modulate leukocytes. Psoriasis is a chronic inflammatory skin disease, characterized by KC hyperproliferation, vasculature growth, and leukocyte infiltration into the dermis and epidermis. Imiquimod (IMQ) is an immunomodulator used in mice to induce lesions closely resembling human psoriasis. The aim of our work was to assess the impact of desmoglein-4 deficiency in the amount of skin leukocyte infiltration in an IMQ induced psoriasis model in rats. To this end, OFA hr/hr rats, which are mutant for the desmoglein-4 gene and Sprague-Dawley (SD) wild type rats were used. IMQ was administered to both strains in shaved skin for four days to generate psoriasis-like lesions. Skin biopsies from treated and untreated OFA and SD rats were weighed and minced to obtain cell suspensions that were stained with monoclonal antibodies against CD45 (panleukocytary lineage) and CD3 (T cell lineage) conjugated with fluorochromes and analyzed by flow cytometry. Interestingly, we found that IMQ treatment to both groups increased CD45+ CD3+ cells in OFA skin compared to controls, but this difference was much greater and significant in OFA rats (SD 0.79±0.24 vs OFA 4.12±0.75, p