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

MORENO SOSA MARÍA TAMARA; PIETROBON ELISA; INNOCENTI BADANO ALICIA CAROLINA ; SOAJE MARTA; VALDEZ SUSANA; SÁNCHEZ MARÍA BELÉN; YÚDICA SEDANO FLORENCIA; NEIRA FLAVIA; PENNACCHIO GISELA; JAHN GRACIELA ALMA; MACKERN OBERTI JUAN PABLO

Buenos Aires

Otro; Reunión Conjunta de Sociedades de Biociencias; 2017

It is known that desmogleins are involved in cell adhesion mechanismsand 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 inflammatoryfactors that modulate leukocytes. Psoriasis is a chronicinflammatory skin disease, characterized by KC hyperproliferation,vasculature growth, and leukocyte infiltration into the dermis andepidermis. Imiquimod (IMQ) is an immunomodulator used in miceto induce lesions closely resembling human psoriasis. The aim ofour work was to assess the impact of desmoglein-4 deficiency inthe amount of skin leukocyte infiltration in an IMQ induced psoriasismodel in rats. To this end, OFA hr/hr rats, which are mutant for thedesmoglein-4 gene and Sprague-Dawley (SD) wild type rats wereused. IMQ was administered to both strains in shaved skin for fourdays to generate psoriasis-like lesions. Skin biopsies from treatedand untreated OFA and SD rats were weighed and minced to obtaincell suspensions that were stained with monoclonal antibodiesagainst 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 increasedCD45+ CD3+ cells in OFA skin compared to controls, but this differencewas much greater and significant in OFA rats (SD 0.79±0.24 vsOFA 4.12±0.75, p