Back to Search Start Over

Immunological synapse formation induces mitochondrial clustering and mitophagy in dendritic cells

Authors :
Michael P. Murphy
Olga Criado-García
José Luis Rodríguez-Fernández
Patricia Boya
Laura Gómez-Cabañas
Pilar López-Cotarelo
Ministerio de Economía y Competitividad (España)
Ministerio de Ciencia, Innovación y Universidades (España)
Instituto de Salud Carlos III
Comunidad de Madrid
Gómez-Cabañas, Laura
López-Cotarelo, Pilar
Boya, Patricia
Murphy, Mike [0000-0003-1115-9618]
Apollo - University of Cambridge Repository
Gómez-Cabañas, Laura [0000-0003-3759-4116]
López-Cotarelo, Pilar [0000-0003-1578-0110]
Boya, Patricia [0000-0003-3045-951X]
Source :
Digital.CSIC. Repositorio Institucional del CSIC, instname
Publication Year :
2019
Publisher :
American Association of Immunologists, 2019.

Abstract

9 p.-8 fig.<br />The immunological synapse (IS) is a superstructure formed during T cell activation at the zone of contact between T cells and dendritic cells (DCs). The IS includes specific molecular components in the T cell and DCs sides that may result in different functionality. Most of the studies on the IS have focused on the T cell side of this structure and, in contrast, the information available on the IS of DCs is sparse. Autophagy is a cellular process involved in the clearance of damaged proteins and organelles via lysosomal degradation. Mitophagy is the selective autophagy of damaged mitochondria. In this study, it is shown that IS formation induces clustering of mitochondria in the IS of DCs and partial depolarization of these organelles. At the IS of the DCs also accumulate autophagy and mitophagy markers, even when the kinase complex mTORC1, an inhibitor of the autophagy, is active. Together the results presented indicate that IS formation induces local clustering of mitochondria and mitophagy, which could be a homeostatic mechanism to control the quality of mitochondria in this region. The data underline the complexity of the regulatory mechanisms operating in the IS of DCs.<br />This work was supported by Grants SAF-2014-53151-R (Ministerio de Economía y Competitividad), SAF2017-83306-R (Ministerio de Ciencia, Innovación y Universidades), RD08/0075 (Red de Inflamación y Enfermedades Reumáticas [Redes Temáticas de Investigación Cooperativa en Salud Program/Instituto de Salud Carlos III]), and S2010/BMD-2350 (Consejería de Educación y Empleo from Comunidad de Madrid [Raphyme]) (to J.L.R.-F.). L.G.-C. and P.L.-C were supported by fellowships Formación del Profesorado Universitario and Formación de Personal Investigador, conferred by the Ministerio de Educación y Ciencia and Ministerio de Economía y Competitividad, respectively. M.P.M. was supported by the Medical Research Council UK (MC_U105663142) and a Wellcome Trust Investigator Award (110159/Z/15/Z).

Details

Language :
English
Database :
OpenAIRE
Journal :
Digital.CSIC. Repositorio Institucional del CSIC, instname
Accession number :
edsair.doi.dedup.....058721a61a5f0a6898d7e332114b7033