Author

E. M. Hessel

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

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

A. Chandra· 1 shared A. G. Richter· 1 shared A. M. Condliffe· 1 shared A.-K. Stark· 1 shared E. Banham-Hall· 1 shared G. Bradley· 1 shared J. Clark· 1 shared J. E. Konkel· 1 shared

Activity by Year

2018-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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1 shared paperImmunology

A. Chandra

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2 papers

Recent·Most cited

Distinct eosinophil subsets are modulated by agonists of the commensal-metabolite and vitamin B3 receptor GPR109A during allergic-type inflammation

R. Azzoni, K. J. Filbey, R. H. Daw, M. Z. Krauss, M. R. Hepworth, J. E. Konkel, E. M. Hessel, Y. Kannan, J. R. Grainger

The paper identifies GPR109A as a regulator of glycolytic Siglec-Fhi eosinophils during allergic inflammation, showing that GPR109A ligands reduce their frequency and activation.

bioRxiv · Aug 4, 2022 · PreprintImmunology

PI3Kδ hyper-activation promotes the development of B cells that exacerbate Streptococcus pneumoniae infection in an antibody-independent manner

A.-K. Stark, A. Chandra, K. Chakraborty, R. Alam, V. Carbonaro, J. Clark, S. Sriskantharajah, G. Bradley, A. G. Richter, E. Banham-Hall, M. R. Clatworthy, S. Nejentsev, J. N. Hamblin, E. M. Hessel, A. M. Condliffe, K. Okkenhaug

This study identifies a PI3Kδ-driven B cell subset in the lungs that worsens Streptococcus pneumoniae infection independently of antibodies, and shows that inhibiting PI3Kδ improves survival.

bioRxiv · Mar 18, 2018Immunology