Author

R. A. Schuepbach

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· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:host-pathogen & immune response· 4 Organism:human· 4 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:flow cytometry· 1

Frequent Co-Authors

A. Gomez-Mejia· 4 shared A. S. Zinkernagel· 4 shared M. Huemer· 4 shared S. D. Brugger· 3 shared S. Mairpady Shambat· 3 shared T. A. Schweizer· 3 shared C. Acevedo· 2 shared C. Vulin· 2 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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4 shared papersMicrobiology

A. Gomez-Mejia

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Alpha-toxin elicited CX3CL1-release via ADAM10 in Staphylococcus aureus pneumoniaimpairs bactericidal function of human monocytes

S. Mairpady Shambat, P. Chen, R. M. Barilla, M. Huemer, J. Snaell, A. Welin, T. S. Cohen, V. Takahashi, S. B. Berry, A. Gomez-Mejia, T. A. Schweizer, D. M. Cunoosamy, S. Cajander, M. Lourdaa, V. Ozenci, , M. Svensson

This study shows that S. aureus alpha-toxin induces CX3CL1 release via ADAM10 in lung epithelium, impairing monocyte bactericidal function through CX3CL1-dependent mechanisms.

bioRxiv · Sep 17, 2023 · PreprintMicrobiology

Group A Streptococcus antibiotic tolerance in necrotizing fasciitis

N. Keller, M. Boumasmoud, F. Andreoni, A. Tarnutzer, M. von Matt, T. C. Scheier, A. Gomez-Mejia, M. Huemer, E. Marques-Maggio, R. A. Schuepbach, S. Mairpady-Shambat, S. D. Brugger, A. S. Zinkernagel

This study shows that Group A Streptococcus (GAS) persisters are present in tissue from necrotizing fasciitis patients and contribute to antibiotic treatment failure.

bioRxiv · Aug 19, 2022 · PreprintMicrobiology

Neutrophil and monocyte dysfunctional effector response towards bacterial challenge in critically-ill COVID-19 patients

S. Mairpady Shambat, A. Gomez-Mejia, T. A. Schweizer, M. Huemer, C.-C. Chang, C. Acevedo, J. Bergada Pijuan, C. Vulin, N. Miroshnikova, D. A. Hofmanner, P. D. Wendel Garcia, M. P. Hilty, P. K. Buehler, R. A. Schuepbach, S. D. Brugger, A. S. Zinkernagel

This study shows that severe hypercytokinemia in COVID-19 patients impairs neutrophil and monocyte function against bacterial challenges, leading to reduced microbicidal capacity and altered receptor signaling.

PLOS Pathogens · Jan 10, 2022Peer-reviewedImmunology

Blunted Fas signaling favors RIPK1-driven neutrophil necroptosis in critically ill COVID-19 patients

T. A. Schweizer, S. Mairpady Shambat, C. Vulin, S. Hoeller, C. Acevedo, M. Huemer, A. Gomez-Mejia, C.-C. Chang, J. Baum, S. Hertegonne, E. Hitz, D. A. Hofmaenner, P. K. Buehler, H. Moch, R. A. Schuepbach, , A. S. Zinkernagel

The paper shows that in critically ill COVID-19 patients, dysregulated Fas signaling leads to increased RIPK1-driven necroptosis in neutrophils, contributing to disease severity.

bioRxiv · Mar 19, 2021 · PreprintImmunology