LRH-1/NR5A2 targets mitochondrial dynamics to reprogram type 1 diabetes macrophages and dendritic cells into an immune tolerance phenotype

The complex aetiology of type 1 diabetes (T1D), characterised by a detrimental cross-talk between the immune system and insulin-producing beta cells, has hindered the development of effective disease-modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can reverse hy...

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Detalles Bibliográficos
Autores: Cobo-Vuilleumier, Nadia, Rodríguez-Fernandez, Silvia, López-Noriega, Livia, Lorenzo, Petra I., Franco, Jaime M., Lachaud, Christian C., Martín-Vázquez, Eugenia, Legido, Raquel Araujo, Dorronsoro, Akaitz, López-Férnandez-Sobrino, Raul, Fernández-Santos, Beatriz, Espejo Serrano, Carmen, Salas-Lloret, Daniel, van Overbeek, Nila, Ramos-Rodriguez, Mireia, Mateo-Rodríguez, Carmen, Hidalgo, Lucia, Marin-Canas, Sandra, Nano, Rita, Arroba, Ana I., Campos Caro, Antonio, Vertegaal, Alfred C. O., Martín-Montalvo, Alejandro, Martín, Franz, Aguilar-Diosdado, Manuel, Piemonti, Lorenzo, Pasquali, Lorenzo, González Prieto, Roman, García Sánchez, Maria Isabel, Eizirik, Decio L., Martínez-Brocca, Maria Asuncion, Vives-Pi, Marta, Gauthier, Benoit R.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/387211
Acceso en línea:http://hdl.handle.net/10261/387211
Access Level:acceso abierto
Palabra clave:Autoimmune diseases
Drug development
Immune tolerance
Pancreatic islets
Descripción
Sumario:The complex aetiology of type 1 diabetes (T1D), characterised by a detrimental cross-talk between the immune system and insulin-producing beta cells, has hindered the development of effective disease-modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can reverse hyperglycaemia in mouse models of T1D by attenuating the autoimmune attack coupled to beta cell survival/regeneration prompted us to investigate whether immune tolerisation could be translated to individuals with T1D by LRH-1/NR5A2 activation and improve islet survival.

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