Author

Landon M. Clark

Vanderbilt UniversityORCID 0000-0002-1537-4692Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:mouse· 2 Research Focus:cell-cell communication· 1 Research Focus:clustering· 1 Assay:flow cytometry· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Lindsay E BassiD· 3 shared Rachel H. BonamiiD· 3 shared C. Mark NicholsiD· 2 shared Dudley H. McNittiD· 2 shared James McAninch· 2 shared Marguerite L Padgett· 2 shared Andres F. Moreno· 1 shared Bryan Han· 1 shared

Activity by Year

2026-2026 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersImmunology

Lindsay E BassORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

ImmunologybioRxivPreprintOct 2, 2026

✦ In-depth digest

Transcriptionally distinct atypical B cell populations contribute to insulin autoreactivity and show differential activation, isotype switching, and somatic hypermutation in early-stage type 1 diabetes individuals

Lindsay E Bass, Landon M. Clark, Bryan Han…·Rachel H. Bonami

B cells from 24 early-stage type 1 diabetes individuals include four atypical clusters differing in switching and mutation; Cluster 10 had the highest insulin-binding antibody rate (5/16).

1 citation

humanscRNA-seq

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ImmunologybioRxivPreprintAug 2, 2026

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…·Rachel H. Bonami

DOI 10.64898/2026.07.29.741363

mouseflow cytometry

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ImmunologyiSciencePeer-reviewedJun 1, 2026

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

Landon M. Clark, James McAninch, Dudley H. McNitt…·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.

1 citation

mouseexperimental assay

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