Author

A. J. Simpson

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

Biology Disciplines

Click to filter author papers

Immunology· 2 Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 4 Organism:human· 3 Assay:bulk RNA-seq· 2 Research Focus:host-pathogen & immune response· 2 Assay:proteomics· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1

Frequent Co-Authors

J. Scott· 3 shared A. Conway Morris· 1 shared A. J. Wood· 1 shared A. K. Long· 1 shared A. M. Vassallo· 1 shared A. Publicover· 1 shared A. Rostron· 1 shared A. S. Mirchandani· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersCell Biology

J. Scott

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Hypoxia shapes the immune landscape in lung injury promoting inflammation persistence

A. S. Mirchandani, S. J. Jenkins, C. C. Bain, H. Lawson, P. Coelho, F. Murphy, D. Griffith, A. Zhang, M. A. Sanchez-Garcia, L. Reyes, T. Morrison, S. Arienti, P. Sadiku, E. Watts, R. Dickinson, , S. Walmsley

This study shows hypoxia suppresses type I interferon signaling in ALI, leading to monocytopenia and unchecked inflammation, which can be mitigated by CSF1 administration.

bioRxiv · Mar 11, 2022 · PreprintCell Biology

A MALDI-TOF assay identifies nilotinib as an inhibitor of inflammation in acute myeloid leukaemia

J. L. Marin-Rubio, R. E. Heap, T. Heunis, M. E. Duenas, J. Inns, J. Scott, A. J. Simpson, J. M. Allan, H. Blair, O. Heidenreich, B. Saxty, M. Trost

This study identifies nilotinib as an anti-inflammatory drug using a MALDI-TOF assay in AML-derived monocytes, showing it inhibits the p38-MK2/3 signaling axis.

bioRxiv · Mar 29, 2021 · PreprintCancer Biology

Complement C5a impairs phagosomal maturation in the neutrophil through phosphoproteomic remodelling.

A. J. Wood, A. M. Vassallo, M.-H. Ruchard-Sparagano, J. Scott, C. Zinnato, C. Gonzalez-Tejedo, K. Kishore, C. D'Santos, A. J. Simpson, D. Menon, C. Summers, E. R. Chilvers, K. Okkenhaug, A. Conway Morris

This study identifies C5a-induced phosphoproteomic changes in human neutrophils that impair phagosomal maturation and acidification, leading to reduced killing of Staphylococcus aureus.

bioRxiv · Jan 17, 2020Immunology

Donor monocyte-derived macrophages promote human acute graft versus host disease

L. Jardine, U. Cytlak, M. Gunawan, G. Reynolds, K. Green, X.-N. Wang, S. Pagan, M. Pradnya, C. A. Lamb, A. K. Long, E. Hurst, S. Nair, G. Jackson, A. Publicover, V. Bigley, , M. Collin

The paper identifies donor monocyte-derived macrophages as key players in human acute graft versus host disease, showing their enhanced activation of T cells and secretion of inflammatory cytokines.

bioRxiv · Sep 30, 2019Immunology