Skewing dendritic cell differentiation towards a tolerogenic state for recovery of tolerance in rheumatoid arthritis

Katina Schinnerling, Lilian Soto, Paulina García-González, Diego Catalán, Juan C. Aguillón

Resultado de la investigación: Contribución a una revistaArtículo de revisiónrevisión exhaustiva

29 Citas (Scopus)

Resumen

To date, the available options to treat autoimmune diseases such as rheumatoid arthritis (RA) include traditional corticoids and biological drugs, which are not exempt of adverse effects. The development of cellular therapies based on dendritic cells with tolerogenic functions (TolDCs) has opened a new possibility to efficiently eradicate symptoms and control the immune response in the field of autoimmunity. TolDCs are an attractive tool for antigen-specific immunotherapy to restore self-tolerance in RA and other autoimmune disorders. A promising strategy is to inject autologous self-antigen-loaded TolDCs, which are able to delete or reprogram autoreactive T cells. Different protocols for the generation of stable human TolDCs have been established and the therapeutic effect of TolDCs has been investigated in multiple rodent models of arthritis. Pilot studies in humans confirmed that TolDC application is safe, encouraging clinical trials using self-antigen-loaded TolDCs in RA patients. Although an abundance of molecular regulators of DC functions has been discovered in the last decade, no master regulator of tolerogenicity has been identified yet. Further research is required to define biomarkers or key regulators of tolerogenicity that might facilitate the induction and monitoring of TolDCs.

Idioma originalInglés
Páginas (desde-hasta)517-527
Número de páginas11
PublicaciónAutoimmunity Reviews
Volumen14
N.º6
DOI
EstadoPublicada - 2015
Publicado de forma externa

Áreas temáticas de ASJC Scopus

  • Inmulogía y alergología
  • Inmunología

Huella

Profundice en los temas de investigación de 'Skewing dendritic cell differentiation towards a tolerogenic state for recovery of tolerance in rheumatoid arthritis'. En conjunto forman una huella única.

Citar esto