Author

Jennifer Londregan

University of PennsylvaniaORCID 0000-0003-2236-3577Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Jeffrey R. MaslankaiD· 3 shared Joseph P. ZackulariD· 2 shared Michael C. AbtiD· 2 shared Mohamad‐Gabriel AlamehiD· 2 shared Brian T. GaudetteiD· 1 shared Dana Borden LacyiD· 1 shared David AllmaniD· 1 shared David B. WeineriD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersImmunology

Jeffrey R. MaslankaORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

ImmunologyThe Journal of ImmunologyPeer-reviewedAug 1, 2026

Generation and characterization of a novel MHC-II tetramer for tracking and characterization of toxin B-specific CD4+ T cell responses

Jeffrey R. Maslanka, Qianxuan She, Kathleen S Krauss…·Michael C. Abt

The paper develops an MHC-II tetramer to track TcdB-specific CD4+ T cells in mice, validating its use in identifying Tfh cells and generating toxin-specific T cells.

1 citationtop 4%

mouseexperimental assay

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ImmunologyCell ReportsPeer-reviewedJul 30, 2026

Notch2 signaling instructs viral and bacterial TLR responsiveness in B cells

Jennifer Londregan, Isaiah Rozich, Brian T. Gaudette…·David Allman

This study shows Notch2 signaling enhances TLR3 and TLR4 responsiveness in MZ B cells, promoting immune responses to viral and bacterial pathogens.

DOI 10.1016/j.celrep.2026.117748

mousebulk RNA-seq

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ImmunologyMucosal ImmunologyPeer-reviewedAug 18, 2025

Clostridioides difficile toxin A and toxin B inhibit toxin-specific adaptive immune responses through glucosyltransferase-dependent activity

Jeffrey R. Maslanka, Jennifer Londregan, Joshua E. Denny…·Michael C. Abt

This study shows that C. difficile toxins A and B inhibit their own antigen-specific immune responses via glucosyltransferase activity, contributing to recurrent infections.

5 citations

mouseproteomics

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