Author

E. Gwyer Findlay

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· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Organism:human· 1 Assay:proteomics· 1

Frequent Co-Authors

D. Minns· 3 shared K. J. Smith· 3 shared D. J. Davidson· 2 shared L. Melrose· 2 shared A. Rossi· 1 shared A. S. MacDonald· 1 shared A. Williams· 1 shared B. McHugh· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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3 shared papersImmunology

D. Minns

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Author profile →

3 papers

Recent·Most cited

The antimicrobial peptide cathelicidin is critical for the development of Th17 responses in severe inflammatory disease

K. J. Smith, D. Minns, B. McHugh, R. Holloway, R. O'Connor, A. Williams, L. Melrose, R. McPherson, V. E. Miron, D. J. Davidson, E. Gwyer Findlay

This study shows cathelicidin promotes Th17 responses and severe EAE by enhancing T cell differentiation and plasticity, and its absence protects mice from disease.

bioRxiv · Jan 27, 2022 · PreprintImmunology

The outcome of neutrophil-T cell contact differs depending on activation status of both cell types

D. Minns, K. J. Smith, G. R. Hardisty, A. Rossi, E. Gwyer Findlay

This study investigates how the activation status of neutrophils and T cells affects their interaction outcomes, finding that resting neutrophils suppress T cell responses while de-granulating neutrophils do not.

bioRxiv · Nov 5, 2020Immunology

The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation

D. Minns, K. J. Smith, V. Alessandrini, G. Hardisty, L. Melrose, L. H. Jackson-Jones, A. S. MacDonald, D. J. Davidson, E. Gwyer Findlay

This study shows cathelicidin promotes Th17 differentiation by enhancing AHR and RORγt expression, increasing IL-17F production, and protecting Th17 cells from apoptosis.

bioRxiv · Apr 10, 2020Immunology