Author

David V. Serreze

Jackson LaboratoryORCID 0000-0001-7614-5925Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

Andrew WalteriD· 1 shared Aron Geurts· 1 shared Chih-Hao ChangiD· 1 shared Daniel A. SkellyiD· 1 shared Deanna J. Lamont· 1 shared Diane Luo· 1 shared Edison T. LiuiD· 1 shared Elise T. CourtoisiD· 1 shared

Activity by Year

2018-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperCancer Biology

Andrew WalterORCID

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2 papers

Recent·Most cited

Cancer BiologyCell ReportsPeer-reviewedMay 1, 2025

Mapping the genetic landscape establishing a tumor immune microenvironment favorable for anti-PD-1 response in mice and humans

Daniel A. Skelly, John P. Graham, Mingshan Cheng…·Edison T. Liu

The paper identifies host genetic factors influencing anti-PD-1 response in mice and humans by mapping QTLs and finding a core gene network with prognostic value in human tumors.

5 citations

mousehuman

𝕏 PostBluesky

ImmunologybioRxivPreprintMar 26, 2018

A hypermorphic Nfkbid allele represents an Idd7 locus gene contributing to impaired thymic deletion of autoreactive diabetogenic CD8+ T-cells in NOD mice.

Maximiliano Presa, Jeremy J. Racine, Jennifer R. Dwyer…·David V. Serreze

This study identifies a hypermorphic Nfkbid allele at the Idd7 locus that impairs thymic deletion of autoreactive CD8+ T-cells in NOD mice, contributing to type 1 diabetes development.

DOI 10.1101/249094

mousegenetic perturbation / CRISPR

𝕏 PostBluesky