Author
Listed:
- Prasanti Kotagiri
(University of Cambridge
University of Cambridge School of Clinical Medicine
Monash University
Stanford University)
- William M. Rae
(University of Cambridge
University of Cambridge School of Clinical Medicine
Cambridge Biomedical Campus)
- Laura Bergamaschi
(University of Cambridge
University of Cambridge School of Clinical Medicine)
- Diana Pombal
(University of Cambridge School of Clinical Medicine)
- Ji-Yeun Lee
(Stanford University)
- Nurulamin M. Noor
(University of Cambridge School of Clinical Medicine)
- Raoul S. Sojwal
(Stanford University)
- Samuel J. S. Rubin
(Stanford University)
- Lukas W. Unger
(University of Cambridge
University of Cambridge School of Clinical Medicine
Medical University of Vienna)
- Sofie H. Tolmeijer
(University of Cambridge School of Clinical Medicine)
- Giulia Manferrari
(University of Cambridge School of Clinical Medicine)
- Rachael J. M. Bashford-Rogers
(University of Cambridge School of Clinical Medicine
University of Oxford)
- David B. Bingham
(Stanford University)
- Anton Stift
(Medical University of Vienna)
- Stephan Rogalla
(Stanford University)
- John Gubatan
(Stanford University)
- James C. Lee
(University of Cambridge
Royal Free Campus)
- Kenneth G. C. Smith
(University of Cambridge
University of Cambridge School of Clinical Medicine)
- Eoin F. McKinney
(University of Cambridge
University of Cambridge School of Clinical Medicine)
- Scott D. Boyd
(Stanford University)
- Paul A. Lyons
(University of Cambridge
University of Cambridge School of Clinical Medicine)
Abstract
B cells have important functions in gut homeostasis, and dysregulated B cell populations are frequently observed in patients with inflammatory bowel diseases, including both ulcerative colitis (UC) and Crohn’s disease (CD). How these B cell perturbations contribute to disease remains largely unknown. Here, we perform deep sequencing of the B cell receptor (BCR) repertoire in four cohorts of patients with CD, together with healthy controls and patients with UC. We identify BCR clones that are shared between patients with CD but not found in healthy individuals nor in patients with UC, indicating CD-associated B cell immune responses. Shared clones are present in the inflamed gut mucosa, draining intestinal lymph nodes and blood, suggesting the presence of common CD-associated antigens that drive B cell responses in CD patients.
Suggested Citation
Prasanti Kotagiri & William M. Rae & Laura Bergamaschi & Diana Pombal & Ji-Yeun Lee & Nurulamin M. Noor & Raoul S. Sojwal & Samuel J. S. Rubin & Lukas W. Unger & Sofie H. Tolmeijer & Giulia Manferrari, 2025.
"Disease-specific B cell clones are shared between patients with Crohn’s disease,"
Nature Communications, Nature, vol. 16(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-58977-y
DOI: 10.1038/s41467-025-58977-y
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