Author

James McAninch

Vanderbilt University

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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Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 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:proteomics· 1

Frequent Co-Authors

C. Mark NicholsiD· 2 shared Dudley H. McNittiD· 2 shared Landon M. ClarkiD· 2 shared Lindsay E BassiD· 2 shared Marguerite L Padgett· 2 shared Rachel H. BonamiiD· 2 shared Andres F. Moreno· 1 shared Christina T Brannon· 1 shared

Activity by Year

2026-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 42 mutual co-author links

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2 shared papersImmunology

C. Mark NicholsORCID

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2 papers

Recent·Most cited

SAP loss limits anti-insulin atypical B cell activation and pro-inflammatory CD8 T cells despite preserved Tfh responses to protect against type 1 diabetes

Landon M. Clark, Dudley H. McNitt, James McAninch, Lindsay E Bass, Marguerite L Padgett, Andres F. Moreno, Christina T Brannon, C. Mark Nichols, Matthew T. Stier, Rachel H. Bonami

bioRxiv · Aug 2, 2026 · PreprintImmunology

BCL6 in T cells promotes type 1 diabetes by redirecting fates of insulin-autoreactive B lymphocytes

Landon M. Clark, James McAninch, Dudley H. McNitt, Marguerite L Padgett, Tyler W. Jenkins, Lindsay E Bass, C. Mark Nichols, Jeffrey C. Rathmell, Rachel H. Bonami

This paper shows that BCL6 in T cells promotes type 1 diabetes by enabling anti-insulin B cells to become pathogenic, and that blocking BCL6 in T cells prevents diabetes even when insulin-reactive B cells are present.

iScience · Jun 1, 2026Peer-reviewedImmunology