Author

L. Shallberg

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 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:development & morphogenesis· 1 Assay:proteomics· 1

Frequent Co-Authors

C. A. Hunter· 3 shared A. P. Hart· 2 shared D. A. Christian· 2 shared J. A. Perry· 2 shared J. T. Clark· 2 shared A. Glatman Zaretsky· 1 shared A. H. Sharpe· 1 shared B. B. Douglas· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 34 mutual co-author links

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3 shared papersImmunology

C. A. Hunter

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

PD-1 and CTLA-4 exert additive control of effector regulatory T cells

J. A. Perry, Z. Lanzar, J. T. Clark, A. P. Hart, B. B. Douglas, L. Shallberg, K. O'Dea, D. A. Christian, C. A. Hunter

This study shows that PD-1 and CTLA-4 pathways additively regulate effector Treg cells by modulating their suppressive function and proliferation.

bioRxiv · Jul 22, 2022 · PreprintImmunology

A positive feedback loop controls Toxoplasma chronic differentiation

M. H. Licon, C. J. Giuliano, S. Chakladar, L. Shallberg, B. S. Waldman, C. A. Hunter, S. Lourido

The paper identifies a positive feedback loop between BFD1 and BFD2 that drives Toxoplasma gondii chronic differentiation.

bioRxiv · Apr 6, 2022Microbiology

PD-L1 - PD-1 interactions limit effector Treg cell populations at homeostasis and during infection

J. A. Perry, J. T. Clark, J. Gullicksrud, J. DeLong, L. Shallberg, B. Douglas, A. P. Hart, C. Konradt, J. Park, A. Glatman Zaretsky, R. de Waal Malefyt, D. A. Christian, A. H. Sharpe, C. A. Hunter

This study shows that PD-L1-PD-1 interactions regulate Treg cell populations at homeostasis and during infection, limiting their numbers to enhance pathogen-specific CD4+ T cell responses.

bioRxiv · Dec 9, 2020 · PreprintImmunology