Author

Michele P. Lambert

Children's Hospital of PhiladelphiaORCID 0000-0003-0439-402XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 1 Genetic & Genomic Medicine· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Assay:flow cytometry· 1 Research Focus:host-pathogen & immune response· 1 Assay:imaging· 1

Frequent Co-Authors

Aime T. FrancoiD· 1 shared Alice Bailey· 1 shared Anne S. BassettiD· 1 shared Bernice E. MorrowiD· 1 shared Beverly S. EmanueliD· 1 shared Chhanda Biswas· 1 shared Chintan Jobaliya· 1 shared Connie JiangiD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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1 shared paperGenetic & Genomic Medicine

Aime T. FrancoORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Cell BiologybioRxivPreprintMay 28, 2026

Hidden Complexity of Pediatric Platelet Disorders: Functional Diversity and Unexpected Hypercoagulable Phenotypes

T.O. Shepelyuk, Evgeniya A. Melnikova, Praharsha Konde…·Ekaterina L. Grishchuk

This study identifies functional diversity and unexpected hypercoagulable phenotypes in pediatric platelet disorders, revealing complexity beyond traditional diagnostic categories.

DOI 10.64898/2026.05.27.728206

humanflow cytometry

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ImmunologyJournal of Leukocyte BiologyPeer-reviewedOct 11, 2024

Transcription Factor NRF2 is Activated by Erythrophagocytosis of Oxidized Red Blood Cell Products and Suppresses the IL-12-IFNg-IL-10 Axis in a Murine Model of Hyperinflammatory Disease

Paul M Gallo, Em Elliott, Grace C Ford…·Edward M. Behrens

This study shows that NRF2 activation by erythrophagocytosis suppresses the IL-12-IFNg-IL-10 axis, reducing hyperinflammation in a murine model of hyperinflammatory disease.

2 citations

mouseproteomics

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Genetic & Genomic MedicineClinical GeneticsPeer-reviewedSep 8, 2022

Platelet findings in 22q11.2 Deletion Syndrome correlate with disease manifestations but do not correlate with GP1b surface expression

Ian M. Campbell, Terrence Blaine Crowley, Chintan Jobaliya…·Michele P. Lambert

The paper examines platelet parameters in 22q11.2 deletion syndrome patients, finding that deletion status of GP1BB, not surface expression, determines platelet counts and that counts decrease with age.

9 citations

humanstatistical model

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