Author

Natalia Athanasiadi

The Francis Crick InstituteORCID 0009-0006-4453-0611Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Maximiliano Gabriel GutierreziD· 2 shared Antony FearnsiD· 1 shared Chak Hon LukiD· 1 shared Claudio BussiiD· 1 shared Enrica PellegrinoiD· 1 shared Gabriel L. Conway· 1 shared Irene Rodríguez Hernández· 1 shared Janick D. Stucki· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersBioengineering

Maximiliano Gabriel GutierrezORCID

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2 papers

Recent·Most cited

BioengineeringScience AdvancesPeer-reviewedJan 1, 2026

✦ In-depth digest

Autologous human iPSC-derived Alveolus-on-Chip reveals early pathological events of M. tuberculosis infection

Chak Hon Luk, Gabriel L. Conway, Kim Jee Goh…·Maximiliano Gabriel Gutierrez

A single-donor iPSC-derived alveolar chip with epithelial, endothelial and macrophage cells models early Mycobacterium tuberculosis infection and shows ATG14-deficient macrophages die more without extra bacterial replication.

10 citationstop 1%

humanbacteria (other)

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Cell BiologymBioPeer-reviewedJul 10, 2024

Physiologic media renders human iPSC-derived macrophages permissive for M. tuberculosis by rewiring organelle function and metabolism

Claudio Bussi, Rachel Lai, Natalia Athanasiadi, Maximiliano Gabriel Gutierrez

This study shows that using a human plasma-like medium enhances M. tuberculosis replication in iPSC-derived macrophages by altering lipid metabolism and organelle function.

15 citationstop 4%

humanbulk RNA-seq

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