Author

F. Pinci

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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Immunology· 2 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 3 Organism:human· 3 Research Focus:cell signaling & trafficking· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

D. Nagl· 2 shared V. Hornung· 2 shared A. Bolleboom· 1 shared A. L. Froehlich· 1 shared B. B. Oude Munnink· 1 shared B. E. Verstrepen· 1 shared C. A. Stafford· 1 shared C. Dirven· 1 shared

Activity by Year

2019-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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2 shared papersImmunology

D. Nagl

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Dissecting MPXV neurotropism and host antiviral signaling using human stem cell-based models

L. Bauer, S. Giussani, N. Palazzi, E. Bot, E. Colombo, F. Zare, F. Pinci, L. Leijten, K. Lanko, F. F. W. Benavides, H. Smeenk, C. W. E. Embregts, J. K. H. Spoor, C. Dirven, Z. Gao, , O. Harschnitz

This study investigates MPXV neurotropism and antiviral signaling in CNS cells using human stem cell-derived models, finding that glial cells are more susceptible and exhibit reduced type I IFN responses.

bioRxiv · Aug 25, 2023 · PreprintMicrobiology

Tumor necrosis factor is a necroptosis-associated alarmin

F. Pinci, M. Gaidt, C. Jung, D. Nagl, G. Kuut, V. Hornung

This study identifies TNF as a necroptosis-associated alarmin by showing that necroptosis promotes TNF translation and release through ADAM protease activation.

bioRxiv · Aug 1, 2022 · PreprintImmunology

Priming enables a NEK7-independent route of NLRP3 activation

N. A. Schmacke, M. M. Gaidt, I. Szymanska, F. O'Duill, C. A. Stafford, D. Chauhan, A. L. Froehlich, D. Nagl, F. Pinci, J. L. Schmid-Burgk, V. Hornung

This study shows that NEK7 is not required for NLRP3 activation in human and murine cells under pro-inflammatory conditions when TAK1-dependent priming is active.

bioRxiv · Oct 9, 2019 · PreprintImmunology