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TitleBiofunctionalized liposomes to monitor rheumatoid arthritis regression stimulated by Interleukin-23 neutralization
Author(s)Lima, Ana Cláudia Fernandes
Campos, Cláudia F.
Cunha, Cristina
Carvalho, Agostinho
Reis, R. L.
Ferreira, Helena Susana Costa Machado
Neves, N. M.
KeywordsAnti-IL-23 antibodies
Gold nanoparticles
IL-17A inhibition
Rheumatoid arthritis
17A inhibition
23 antibodies
Issue dateJan-2021
JournalAdvanced Healthcare Materials
CitationLima Ana C., Campos C. F., Cunha C., Carvalho A., Reis R. L., Ferreira H., Neves N. M. Biofunctionalized Liposomes to Monitor Rheumatoid Arthritis Regression Stimulated by Interleukin-23 Neutralization, Advanced Healthcare Materials, doi:10.1002/adhm.202001570, 2020
Abstract(s)Even after the revolution of rheumatoid arthritis (RA) treatment with biologic agents, this debilitating disease remains a major clinical problem. The outstanding outcomes of the systemic administration of antibodies (Abs) are narrowed by the risk of serious side effects and limited efficacy due to their short half-life. Interleukin-23 (IL-23) is a crucial pro-inflammatory cytokine involved in inflammation that potently enhances the generation of T-helper type-17 (Th17) cells. Hence, in this work, anti-IL-23 Abs are immobilized at the surface of liposomes to increase their therapeutic efficacy, being gold nanoparticles (AuNPs) incorporated to allow monitoring the biodistribution of the liposomes after systemic administration as well as due to their anti-inflammatory and antioxidant effects. A stable monodispersed liposomesâ suspension with around 130 nm is produced and efficiently biofunctionalized with anti-IL-23 Abs. IL-23 capture and neutralization capacity are confirmed using activated macrophages. Biological assays demonstrate their hemocompatibility and cytocompatibility with human articular chondrocytes, macrophages, and endothelial cells. Moreover, the neutralization of IL-23 by the biofunctionalized liposomes efficiently decreases the production of IL-17A by peripheral blood mononuclear cells of healthy donors and RA patients who are activated to Th17 differentiation. Therefore, the developed formulation may be a promising strategy to treat RA.
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Appears in Collections:3B’s - Artigos em revistas/Papers in scientific journals

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