Author

J. Nunes

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:host-pathogen & immune response· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

D. Olive· 4 shared G. Guittard· 3 shared P.-L. Bernard· 2 shared R. Castellano· 2 shared S. Pastor· 2 shared V. Laletin· 2 shared A. Goubard· 1 shared A. Krug· 1 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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4 shared papersImmunology

D. Olive

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Anti-HVEM mAb therapy improves antitumoral immunity both in vitro and in vivo, in a novel transgenic mouse model expressing human HVEM and BTLA molecules challenged with HVEM expressing tumors

C. Demerle, L. Gorvel, M. Mello, S. Pastor, C. Degos, A. Zarubica, F. Angelis, F. FIORE, J. Nunes, B. Malissen, L. Greillier, G. Guittard, H. Luche, F. Barlesi, D. Olive

bioRxiv · Nov 4, 2022 · PreprintImmunology

CD47-SIRPα controls ADCC killing of primary T cells by PMN through a combination of trogocytosis and NADPH oxidase activation.

F. Gondois-Rey, T. Miller, J. Nunes, D. Olive

This study shows anti-CD47 mAbs induce PMN-mediated T cell killing via trogocytosis and NADPH oxidase activation, highlighting the need to consider PMNs in CD47-SIRP checkpoint therapy.

bioRxiv · Mar 8, 2022Immunology

DOK1 and DOK2 regulate CD8+ T cell signaling and memory formation without affecting tumor cell killing

V. Laletin, P.-L. Bernard, M. Camille, Y. Yamanashi, D. Olive, R. Castellano, G. Guittard, J. Nunes

This study shows that DOK1 and DOK2 inhibit CD8+ T cell memory formation but not tumor cell killing, enhancing TCR signaling without improving cytotoxicity.

bioRxiv · Dec 17, 2021Immunology

Targeting CISH enhances natural cytotoxicity receptor signaling and reduces NK cell exhaustion to improve solid tumor immunity

P.-L. Bernard, R. Delconte, S. Pastor, V. Laletin, C. Costa Da Silva, A. Goubard, E. Josselin, R. Castellano, A. Krug, J. Vernerey, R. Devillier, D. Olive, E. Verhoeyen, E. Vivier, N. Huntington, , G. Guittard

This study shows that deleting CISH enhances NK cell activation and anti-tumor responses in both mice and human cells, suggesting CISH as a therapeutic target for improving NK cell immunotherapy.

bioRxiv · Mar 16, 2021Immunology