Mass cytometry reveals systemic and local immune signatures that distinguish inflammatory bowel diseases

Samuel J. S. Rubin, Lawrence Bai, Yeneneh Haileselassie, Gotzone Garay, Chohee Yun, Laren Becker, Sarah E. Streett, Sidhartha R. Sinha and Aida Habtezion ()
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Samuel J. S. Rubin: Immunology Program, Stanford University School of Medicine
Lawrence Bai: Immunology Program, Stanford University School of Medicine
Yeneneh Haileselassie: Stanford University School of Medicine
Gotzone Garay: Stanford University School of Medicine
Chohee Yun: Stanford University School of Medicine
Laren Becker: Stanford University School of Medicine
Sarah E. Streett: Stanford University School of Medicine
Sidhartha R. Sinha: Stanford University School of Medicine
Aida Habtezion: Immunology Program, Stanford University School of Medicine

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Inflammatory bowel disease (IBD) includes Crohn’s disease and ulcerative colitis. Each disease is characterized by a diverse set of potential manifestations, which determine patients’ disease phenotype. Current understanding of phenotype determinants is limited, despite increasing prevalence and healthcare costs. Diagnosis and monitoring of disease requires invasive procedures, such as endoscopy and tissue biopsy. Here we report signatures of heterogeneity between disease diagnoses and phenotypes. Using mass cytometry, we analyze leukocyte subsets, characterize their function(s), and examine gut-homing molecule expression in blood and intestinal tissue from healthy and/or IBD subjects. Some signatures persist in IBD despite remission, and many signatures are highly represented by leukocytes that express gut trafficking molecules. Moreover, distinct systemic and local immune signatures suggest patterns of cell localization in disease. Our findings highlight the importance of gut tropic leukocytes in circulation and reveal that blood-based immune signatures differentiate clinically relevant subsets of IBD.

Date: 2019
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DOI: 10.1038/s41467-019-10387-7

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