IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
DESMOGLEIN-4 DEFICIENCY ENHANCES SKIN LESIONS IN A RAT PSORIASIS MODEL
Autor/es:
SANCHEZ B; INOCCENTI-BADANO CAROLINA; PIETROBON E; MACKERN JUAN PABLO; MORENO SOSA TAMARA; GRACIELA A. JAHN
Lugar:
Mar del Plata
Reunión:
Congreso; reunion cientifica anual SAIC, SAFE, SAFIS; 2018
Institución organizadora:
SAIC, SAFE, SAFIS
Resumen:
Psoriasis is a chronic inflammatory skin disease,characterized by keratinocyte hyperproliferation,vasculature growth and leukocyte infiltration into thedermis and epidermis. Keratinocytes (KC) produce severalinflammatory factors that modulate leukocytes. It is knownthat desmogleins are proteins present in keratinocytesinvolved in cell adhesion mechanisms and are crucial inkeeping structural integrity of different tissues, includingskin. They also play important roles in differentiation, cellactivation and migration, but their role in psoriasis has notbeen addressed. The aim of our work was to assess theimpact of desmoglein-4 deficiency in the immunologicalresponse of the skin.Figure 2. Dsg4deficiency enhancespro- and antiinflamatorygenesmRNA expression.Pro-inflammatory genesmRNA A. IL-1b, B. IL-8, C. IL-17 and D.TNFa; and antiinflamatorygenes: E.IL-10 and F. TGFb; G.Chemokine geneRANTES and H.Ratio between TGFband IL-17 expressionwere measured by q-PCR and statisticallyanalyzed with 2 wayANOVA and t-TestSD OFAFigure 3. Dsg4 deficiency enhances the expression of chemokine receptors. A. CCR1, B. CCR2, C. CCR3, D. CCR5 and E. CXCR5 mRNA expression were measured by q-PC and statisticallyanalyzed by 2 way ANOVA and t-Test.A B C D