SKIN IMMUNE SYSTEM DIALOG IN AN IN VITRO MODEL: EFFECTS OF ACTIVATED LYMPHOCYTES ON NORMAL KERATINOCYTES PROLIFERATION AND CYTOKINE PRODUCTION.

PAZ, MARIELA LAURA; LEONI, JULIANA; GONZALEZ MAGLIO, DANIEL H

Cordoba

Congreso; LXI Reunión Anual de la Sociedad Argentina de Inmunología; 2013

Sociedad Argentina de Inmunologìa

28. SKIN IMMUNE SYSTEM DIALOG IN AN IN VITRO MODEL: EFFECTS OF ACTIVATED LYMPHOCYTES ON NORMAL KERATINOCYTES PROLIFERATION AND CYTOKINE PRODUCTION.  Skin immune system, composed by cells and soluble molecules, can reach a state of disequilibrium originating chronic inflammatory pathologies (CIP), like psoriasis or atopic dermatitis. We aim to study the interaction of the cutaneous epithelium, particularly keratinocytes (KCs), with the immune system, particularly T helper cells. We generated a KCs primary cell culture from C57 mice epidermis, and we polyclonally activated T cells from a C57 mice spleen with Concanavalin A. We evaluated the effects of activated T cells secreted molecules (supernatant transference) and also the ones of Tcell -KCs contact (coculture: coc) on KCs. Cocs were performed with T cells preactivated 48 hs before or during the cocs (in situ) We measured KCs proliferation by flow cytometry with CFSE probe and KCs cytokine production by ELISA. KCs cytokine concentrations were calculated subtracting the values obtained for activated T cells alone to the ones obtained in the cocs. T cells supernatant transference produced no significant effect on KCs proliferation or cytokine production. Cocs of KCs with preactivated T cells had no influence on KCs proliferation but induced a significant increment in TNF-α production (p<0.001) with respects to the control. Cocs with in situ activated T cells also produced no significant effect on proliferation but indeed stimulated the production of the four cytokines measured with a significant difference respects to the corresponding control (T test): TNF-α (p<0.05), IL-6 (p<0.001), IL-10 (p<0.05) and IFN-γ (p<0.01). Normal KCs seem to become activated by the contact with activated T cells and not by the molecules produced by them. Activated KCs produce inflammatory (TNF-α, IL-6) and regulatory (IL-10) cytokines that lead not only to skin inflammation, but also to a positive feedback activating other T cells which produce more cytokines (IFN-γ, among others), activating further KCs. This might be the way the inflammatory loop is perpetuated in CIP.