Author

M. Lotem

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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Cancer Biology· 1 Immunology· 1 Physiology· 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:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Organism:human· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Veillette· 2 shared E. Hajaj· 2 shared G. Eisenberg· 2 shared J. E. Cohen· 2 shared N. Hacohen· 2 shared S. Frankenburg· 2 shared S. Klein· 2 shared S. Merims· 2 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersImmunology

A. Veillette

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

RORc expressing immune cells negatively regulate tertiary lymphoid structure formation and support their pro-tumorigenic functions

E. Cinnamon, I. Stein, E. Zino, S. Rabinovich, Y. Shovman, Y. Schlesinger, T. M. Salame, S. Reich-Zeliger, M. Lotem, Y. Ben-Neriah, O. Parnas, E. Pikarsky

This study shows RORc-expressing immune cells suppress tertiary lymphoid structure (TLS) formation in liver cancer, leading to pro-tumorigenic TLSs, while their absence results in anti-tumorigenic TLSs.

bioRxiv · Jul 2, 2022Cancer Biology

Alternative splicing of SLAMF6 in human T cells creates a co-stimulatory isoform that counteracts the inhibitory effect of the full-length receptor

E. Hajaj, E. Zisman, S. Tzaban, S. Merims, J. E. Cohen, S. Klein, S. Frankenburg, M. Sade-Feldman, Y. Tabach, K. Yizhak, A. Navon, P. Stepensky, N. Hacohen, T. Peretz, A. Veillette, , M. Lotem

This study identifies an alternative splicing event in SLAMF6 that generates a co-stimulatory isoform, which enhances T cell cytotoxicity and is associated with improved anti-tumor responses in melanoma.

bioRxiv · Aug 21, 2020 · PreprintImmunology

SLAMF6 deficiency augments tumor killing and skews towards an effector phenotype revealing it as a new T cell checkpoint

E. Hajaj, G. Eisenberg, S. Klein, S. Frankenburg, S. Merims, I. Ben David, T. Eisenhaure, S. E. Henrickson, A. C. Villani, N. Hacohen, N. Abudi, R. Abramovich, J. E. Cohen, T. Peretz, A. Veillette, M. Lotem

This study shows that SLAMF6 deficiency enhances T cell tumor-killing ability and shifts T cells toward an effector phenotype, suggesting SLAMF6 as a new immune checkpoint.

bioRxiv · Oct 31, 2019Physiology