2026-04-13T14:01:10Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1732282025-12-05T12:18:28Zcom_2072_1057col_2072_478916col_2072_478917

00925njm 22002777a 4500 dc Hurtado Guerrero, Isaac author Hernáez, Bruno author Pinto Medel, María J. author Calonge, Esther author Rodríguez Bada, José L. author Urbaneja, Patricia author Alonso, Ana author Mena Vázquez, Natalia author Aliaga, Pablo author Issazadeh Navikas, Shohreh author Pavia, José author Leyva, Laura author Alcamí, Antonio author Alcamí, José author Fernández, Óscar author Oliver Martos, Begoña author 2021-01-19T18:15:34Z 2021-01-19T18:15:34Z 2020-04-01 2020-12-21T13:11:24Z Soluble receptors of cytokines are able to modify cytokine activities and therefore the immune system, and some have intrinsic biological activities without mediation from their cytokines. The soluble interferon beta (IFN-ss) receptor is generated through alternative splicing of IFNAR2 and has both agonist and antagonist properties for IFN-ss, but its role is unknown. We previously demonstrated that a recombinant human soluble IFN-ss receptor showed intrinsic therapeutic efficacy in a mouse model of multiple sclerosis. Here we evaluate the potential biological activities of recombinant sIFNAR2 without the mediation of IFN-ss in human cells. Recombinant sIFNAR2 down-regulated the production of IL-17 and IFN-? and reduced the cell proliferation rate. Moreover, it showed a strong antiviral activity, fully protecting the cell monolayer after being infected by the virus. Specific inhibitors completely abrogated the antiviral activity of IFN-ss, but not that of the recombinant sIFNAR2, and there was no activation of the JAK-STAT signaling pathway. Consequently, r-sIFNAR2 exerts immunomodulatory, antiproliferative and antiviral activities without IFN-ss mediation, and could be a promising treatment against viral infections and immune-mediated diseases. Immunologia Interferó Immunology Interferon Antiviral, Immunomodulatory and Antiproliferative Activities of Recombinant Soluble IFNAR2 without IFN-beta Mediation