Author

D. Hudesman

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

P. Loke· 3 shared A. Hine· 2 shared K. Cadwell· 2 shared A. Korman· 1 shared C. Zhou· 1 shared D. Ercelen· 1 shared D. Li· 1 shared D. R. Jones· 1 shared

Activity by Year

2019-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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3 shared papersImmunology

P. Loke

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Author profile →

3 papers

Recent·Most cited

Tofacitinib uptake by patient-derived intestinal organoids predicts individual clinical responsiveness

K. K. Jang, D. Ercelen, J. Y. C. Cen Feng, S. Gurunathan, C. Zhou, A. Korman, L. Newell, D. Hudesman, D. R. Jones, P. Loke, J. E. Axelrad, K. Cadwell

This study uses patient-derived intestinal organoids to predict individual clinical responsiveness to tofacitinib in ulcerative colitis by assessing drug sensitivity and MATE1 expression.

bioRxiv · Mar 2, 2024Cell Biology

Transcriptional Atlas of Ileal-Anal Pouch Immune Cells from Ulcerative Colitis Patients

J. C. Devlin, J. Axelrad, A. Hine, S. Chang, S. Sarkar, J.-D. Lin, K. V. Ruggles, D. Hudesman, K. Cadwell, P. Loke

The paper uses single-cell RNA-sequencing to analyze immune cells in ileal pouches and colons of UC patients, identifying specific cell types and their association with inflammation and treatment response.

bioRxiv · Jul 31, 2020Immunology

Serum Amyloid A Proteins Induce Pathogenic TH17 Cells and Promote Inflammatory Disease

J.-Y. Lee, J. A. Hall, L. Kroehling, L. Wu, T. Najar, H. H. Nguyen, W.-Y. Lin, S. T. Yeung, H. M. Silva, D. Li, A. Hine, P. Loke, D. Hudesman, J. C. Martin, E. Kenigsberg, , D. R. Littman

This study shows serum amyloid A proteins drive pathogenic TH17 cell differentiation and promote inflammatory disease through STAT3-activating cytokines.

bioRxiv · Jun 25, 2019Immunology