Mackern-Oberti, Juan P.Llanos, CarolinaRiedel, Claudia A.Bueno, Susan M.Kalergis, Alexis M.2023-06-192023-06-192015-12Immunology. Volume 146, Issue 4, Pages 497 - 507. 1 December 20150019-2805https://repositorio.unab.cl/xmlui/handle/ria/50826Indexación Scopus.Systemic lupus erythematosus (SLE) is a heterogeneous disease in which excessive inflammation, autoantibodies and complement activation lead to multisystem tissue damage. The contribution of the individual genetic composition has been extensively studied, and several susceptibility genes related to immune pathways that participate in SLE pathogenesis have been identified. It has been proposed that SLE takes place when suscepti bility factors interact with environmental stimuli leading to a deregulated immune response. Experimental evidence suggests that such events are related to the failure of T-cell and B-cell suppression mediated by defects in cell signalling, immune tolerance and apoptotic mechanism promoting autoimmunity. In addition, it has been reported that dendritic cells (DCs) from SLE patients, which are crucial in the modulation of peripheral tol erance to self-antigens, show an increased ratio of activating/inhibitory receptors on their surfaces. This phenotype and an augmented expression of co-stimulatory molecules is thought to be critical for disease pathogen esis. Accordingly, tolerogenic DCs can be a potential strategy for develop ing antigen-specific therapies to reduce detrimental inflammation without causing systemic immunosuppression. In this review article we discuss the most relevant data relative to the contribution of DCs to the triggering of SLE.enDendritic CellsImmune ToleranceImmunotherapyLupusSystemic AutoimmunityArtículoAtribution 4.0 International (CC BY 4.0)10.1111/imm.12504