Author

T. Riffelmacher

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Assay:metabolomics· 3 Organism:mouse· 3 Research Focus:differential expression· 2 Organism:human· 2 Research Focus:metabolism & bioenergetics· 2 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

A. K. Simon· 2 shared A. Chawla· 1 shared A. J. Clarke· 1 shared A. L. R. Premlal· 1 shared C. H. Ottensmeier· 1 shared C. Ramirez-Suastegui· 1 shared C.-H. Lin· 1 shared D. Braas· 1 shared

Activity by Year

2017-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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2 shared papersCell Biology

A. K. Simon

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Author profile →

3 papers

Recent·Most cited

Transcriptomes and metabolism define mouse and human MAIT cell heterogeneity

S. Chandra, G. Ascui, T. Riffelmacher, A. Chawla, C. Ramirez-Suastegui, V. C. Castelan, G. Seumois, H. Simon, M. P. Murray, G.-Y. Seo, A. L. R. Premlal, G. Verstichel, Y. Li, C.-H. Lin, J. Greenbaum, , M. Kronenberg

This study identifies MAIT cell heterogeneity in mice and humans through single-cell RNA sequencing and metabolic analysis, revealing distinct transcriptomes and metabolic states in different tissues and species.

bioRxiv · Dec 20, 2021 · PreprintImmunology

Translational control of TFEB and autophagy via eIF5A rejuvenates B cell immunity

H. Zhang, G. Alsaleh, J. Feltham, Y. Sun, T. Riffelmacher, P. Charles, L. Frau, Z. Yu, S. Mohammed, S. Balabanov, J. Mellor, A. K. Simon

This study identifies a mechanism by which spermidine regulates autophagy through eIF5A-mediated TFEB translation, improving B cell immunity in aging.

bioRxiv · Dec 12, 2018 · PreprintCell Biology

B1a B cells require autophagy for metabolic homeostasis and self-renewal

A. J. Clarke, T. Riffelmacher, D. Braas, R. J. Cornall, A. K. Simon

This study shows B1a B cells rely on autophagy for metabolic homeostasis and self-renewal, with Atg7 deletion causing their loss due to metabolic dysregulation and mitochondrial dysfunction.

bioRxiv · Dec 28, 2017Immunology