Mass cytometry reveals systemic and local immune signatures that distinguish inflammatory bowel diseases
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 hea...
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Published in | Nature communications Vol. 10; no. 1; pp. 2686 - 14 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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London
Nature Publishing Group UK
19.06.2019
Nature Publishing Group Nature Portfolio |
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Online Access | Get full text |
ISSN | 2041-1723 2041-1723 |
DOI | 10.1038/s41467-019-10387-7 |
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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.
Distinguishing clinical subtypes of IBD is critical for optimal treatments, outcome prediction, and better understanding of disease pathogenesis. Here the authors phenotype blood and intestinal immune cells by mass cytometry and identify signatures associated with distinct disease states. |
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AbstractList | 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.
Distinguishing clinical subtypes of IBD is critical for optimal treatments, outcome prediction, and better understanding of disease pathogenesis. Here the authors phenotype blood and intestinal immune cells by mass cytometry and identify signatures associated with distinct disease states. Distinguishing clinical subtypes of IBD is critical for optimal treatments, outcome prediction, and better understanding of disease pathogenesis. Here the authors phenotype blood and intestinal immune cells by mass cytometry and identify signatures associated with distinct disease states. 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. 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.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. |
ArticleNumber | 2686 |
Author | Yun, Chohee Rubin, Samuel J. S. Sinha, Sidhartha R. Bai, Lawrence Habtezion, Aida Becker, Laren Streett, Sarah E. Haileselassie, Yeneneh Garay, Gotzone |
Author_xml | – sequence: 1 givenname: Samuel J. S. orcidid: 0000-0001-7335-3868 surname: Rubin fullname: Rubin, Samuel J. S. organization: Immunology Program, Stanford University School of Medicine, Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine – sequence: 2 givenname: Lawrence orcidid: 0000-0002-5617-9025 surname: Bai fullname: Bai, Lawrence organization: Immunology Program, Stanford University School of Medicine, Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine – sequence: 3 givenname: Yeneneh surname: Haileselassie fullname: Haileselassie, Yeneneh organization: Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine – sequence: 4 givenname: Gotzone surname: Garay fullname: Garay, Gotzone organization: Stanford Center for Clinical Research, Department of Medicine, Stanford University School of Medicine – sequence: 5 givenname: Chohee surname: Yun fullname: Yun, Chohee organization: Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Clinical Research – Inflammation and Respiratory Therapeutic Area, Gilead Sciences – sequence: 6 givenname: Laren surname: Becker fullname: Becker, Laren organization: Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine – sequence: 7 givenname: Sarah E. surname: Streett fullname: Streett, Sarah E. organization: Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine – sequence: 8 givenname: Sidhartha R. orcidid: 0000-0001-5104-6410 surname: Sinha fullname: Sinha, Sidhartha R. organization: Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine – sequence: 9 givenname: Aida surname: Habtezion fullname: Habtezion, Aida email: aidah@stanford.edu organization: Immunology Program, Stanford University School of Medicine, Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31217423$$D View this record in MEDLINE/PubMed |
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Suppl W Reinisch (10387_CR46) 2015; 64 BG Feagan (10387_CR49) 2013; 369 WA Haynes (10387_CR60) 2017; 22 TL Hedrick (10387_CR33) 2013; 26 W Wang (10387_CR39) 2000; 275 A Kessel (10387_CR53) 2012; 11 M Dobre (10387_CR15) 2017; 58 HH Van Acker (10387_CR21) 2017; 8 MS Silverberg (10387_CR8) 2005; 19 C Gasche (10387_CR6) 2000; 6 S Moir (10387_CR29) 2008; 205 V van Unen (10387_CR51) 2016; 44 LP Nguyen (10387_CR18) 2015; 16 S Danese (10387_CR47) 2015; 64 Z Vadasz (10387_CR54) 2013; 587 SC Bendall (10387_CR14) 2012; 33 W Hueber (10387_CR48) 2012; 61 FA Frizelle (10387_CR32) 1997; 12 10387_CR1 CW Lees (10387_CR52) 2011; 60 BR Yacyshyn (10387_CR43) 1993; 34 C Wei (10387_CR28) 2007; 178 SM Jackson (10387_CR56) 2007; 110 JF Fecteau (10387_CR26) 2006; 177 N Samusik (10387_CR58) 2016; 13 J Marsal (10387_CR5) 2012; 272 C Abraham (10387_CR2) 2009; 361 PM Nguyen (10387_CR44) 2015; 35 A Habtezion (10387_CR13) 2016; 150 CE Egwuagu (10387_CR36) 2009; 47 YQ Qiao (10387_CR24) 2013; 20 VJ McGovern (10387_CR11) 1968; 9 P Bekker (10387_CR41) 2015; 2015 10387_CR57 J Bilsborough (10387_CR3) 2016; 3 PJ Trivedi (10387_CR40) 2016; 68 AN Ananthakrishnan (10387_CR4) 2015; 12 X Wang (10387_CR35) 2017; 25 SJ Fleischer (10387_CR27) 2014; 66 J Galvez (10387_CR37) 2014; 2014 AM Newman (10387_CR59) 2015; 12 RK Yantiss (10387_CR10) 2006; 48 K Muroi (10387_CR20) 1998; 22 YC Wu (10387_CR25) 2011; 2 SA Islam (10387_CR12) 2012; 18 OL Rojas (10387_CR30) 2008; 380 MC Jaimes (10387_CR38) 2004; 78 SV Kim (10387_CR17) 2013; 340 WJ Sandborn (10387_CR50) 2013; 369 10387_CR23 B Safar (10387_CR7) 2007; 20 DA Rao (10387_CR34) 2017; 542 X Bing (10387_CR55) 2018; 2018 10387_CR16 S Brand (10387_CR22) 2009; 58 RW Morrison (10387_CR19) 2002; 2310 G Pickert (10387_CR45) 2009; 206 S Mills (10387_CR31) 2007; 20 J Satsangi (10387_CR9) 2006; 55 BR Yacyshyn (10387_CR42) 1995; 108 |
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Snippet | Inflammatory bowel disease (IBD) includes Crohn’s disease and ulcerative colitis. Each disease is characterized by a diverse set of potential manifestations,... Inflammatory bowel disease (IBD) includes Crohn's disease and ulcerative colitis. Each disease is characterized by a diverse set of potential manifestations,... Distinguishing clinical subtypes of IBD is critical for optimal treatments, outcome prediction, and better understanding of disease pathogenesis. Here the... |
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Title | Mass cytometry reveals systemic and local immune signatures that distinguish inflammatory bowel diseases |
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