Journal article

XCR1( ) dendritic cells promote memory CD8( ) T cell recall upon secondary infections with Listeria monocytogenes or certain viruses

Yannick O Alexandre, Sonia Ghilas, Cindy Sanchez, Agnes Le Bon, Karine Crozat, Marc Dalod

Journal of Experimental Medicine | ROCKEFELLER UNIV PRESS | Published : 2016

Abstract

Naive CD8(+) T cell priming during tumor development or many primary infections requires cross-presentation by XCR1(+) dendritic cells (DCs). Memory CD8(+) T lymphocytes (mCTLs) harbor a lower activation threshold as compared with naive cells. However, whether their recall responses depend on XCR1(+) DCs is unknown. By using a new mouse model allowing fluorescent tracking and conditional depletion of XCR1(+) DCs, we demonstrate a differential requirement of these cells for mCTL recall during secondary infections by different pathogens. XCR1(+) DCs were instrumental to promote this function upon secondary challenges with Listeria monocytogenes, vesicular stomatitis virus, or Vaccinia virus, b..

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Grants

Awarded by Agence Nationale de la Recherche


Awarded by Fondation pour la Recherche Medicale (label "Equipe FRM")


Awarded by European Research Council under the European Community's Seventh Framework Program (FP7)


Funding Acknowledgements

We thank Bruno Estebe, Frederic Fiore, and Bernard Malissen (Centre d'Immunophenomique [CIPHE], UM2 Aix-Marseille Universite, Institut National de la Sante et de la Recherche Medicale US012, Centre National de la Recherche Scientifique UMS3367, Marseille, France) for generating the Karma mice; Marilyn Boyron, and the cytometry and ImagImm core facilities (CIML, UMR7280, France) for technical assistance; Mathieu Fallet (CIML, UMR7280, France) for programming macros to quantify memory OT-I cell clustering and migration into the T cell zone; and Toby Lawrence and Elena Tomasello for critical reading of the manuscript. We acknowledge France-BioImaging infrastructure supported by the Agence Nationale de la Recherche (ANR-10-INSB-04-01, call "Investissements d'Avenir").This work was supported by institutional funding from CNRS and Inserm, by the Innate Immunocytes in Health and Disease (I2HD) collaborative project between CIML, AVIESAN, and SANOFI, and by grants from Association pour la recherche sur le cancer (ARC), from Fondation pour la Recherche Medicale (label "Equipe FRM 2011", project number DEQ20110421284) and from the European Research Council under the European Community's Seventh Framework Program (FP7/2007-2013 grant agreement number 281225). Y.O. Alexandre was supported by doctoral fellowships from the French Ministere de l'Enseignement Superieur et de la Recherche, and from ARC. S. Ghilas was laureate from a "University President" Excellence Ph.D. Fellowship from Aix Marseille Universite and from ARC. C. Sanchez was supported by the I2HD CIML-SANOFI project.