Author

M. I. Khalil

National Research CentreORCID 0000-0002-8331-1490Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

M. I. Khalil5 papers

Biology Disciplines

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Cancer Biology· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 3 Research Focus:host-pathogen & immune response· 3 Approach:experimental assay· 2 Organism:human· 2 Organism:mouse· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

Canchai YangiD· 2 shared Craig C. WelboniD· 2 shared Dohun PyeoniD· 2 shared Lexi VuiD· 2 shared William Charles SpanosiD· 2 shared Abigail Z. BennettiD· 1 shared Andrew J. OliveiD· 1 shared Angela K. BeltrameiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCancer Biology

Canchai YangORCID

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3 papers

Recent·Most cited

ULK1 drives NDP52-mediated selective autophagic degradation of MHC-I to promote immune evasion in HPV-positive head and neck cancer

Lexi Vu, Nicholas S. Giacobbi, M. I. Khalil, Canchai Yang, Will Eckerman, Evelyn Gomez Recinos, Johnathon D. Garber, Hyomin Son, Prerna Chahal, Dara M Villa, Tasha Srivastava, Abigail Z. Bennett, Katie R. Martin, Craig C. Welbon, Caitlin S. Williamson, , Dohun Pyeon

This study identifies ULK1-driven autophagy as a mechanism by which HPV+ HNC cells degrade MHC-I, promoting immune evasion and tumor growth.

bioRxiv · Mar 18, 2026 · PreprintCancer Biology

The membrane-associated ubiquitin ligase MARCHF8 promotes cancer immune evasion by degrading MHC class I proteins

M. I. Khalil, Jie Wang, Lexi Vu, Canchai Yang, C. Yin, Smriti Chadha, Harrison Nabors, Daniel B. Vocelle, Danielle G. May, Rachel J. Chrisopulos, Craig C. Welbon, Li Zhou, Kyle J. Roux, William Charles Spanos, Matthew P. Bernard, , Dohun Pyeon

This study identifies MARCHF8 as a driver of cancer immune evasion by degrading MHC-I proteins and shows its inhibition enhances antitumor immunity and response to immunotherapy.

Proceedings of the National Academy of Sciences · Mar 9, 2026Peer-reviewedCancer Biology

Overexpression of GITRL by B cell IgD low (BDL) B cells is a therapeutic strategy to increase endogenous CD4+Foxp3+ T regulatory cells for the treatment of autoimmunity

M. I. Khalil, Cody J. Gurski, Robert Burns, Ryan Zander, Kelli C Sommers, Angela K. Beltrame, Bonnie N. Dittel

This study shows overexpressing GITRL on BDL B cells increases Treg numbers and reduces EAE severity in mice, suggesting a therapeutic strategy for autoimmunity.

bioRxiv · Feb 4, 2025 · PreprintImmunology