Contribution of dendritic cells to the autoimmune pathology of systemic lupus erythematosus
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Fecha
2015-12
Autores
Mackern-Oberti, Juan P.
Llanos, Carolina
Riedel, Claudia A.
Bueno, Susan M.
Kalergis, Alexis M.
Profesor/a Guía
Facultad/escuela
Idioma
en
Título de la revista
ISSN de la revista
Título del volumen
Editor
Blackwell Publishing Ltd
Nombre de Curso
Licencia CC
Atribution 4.0 International (CC BY 4.0)
Licencia CC
https://creativecommons.org/licenses/by/4.0/deed.es
Resumen
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.
Notas
Indexación Scopus.
Palabras clave
Dendritic Cells, Immune Tolerance, Immunotherapy, Lupus, Systemic Autoimmunity
Citación
Immunology. Volume 146, Issue 4, Pages 497 - 507. 1 December 2015
DOI
10.1111/imm.12504