Transcriptional programs of lymphoid tissue capillary and high endothelium reveal control mechanisms for lymphocyte homing

High endothelial vessels (HEVs) provide the conduit for blood-borne leukocytes to enter lymph nodes. Butcher and colleagues report transcriptional profiles of various endothelial cell populations that can explain functional differences of homing-molecule modifications. Lymphocytes are recruited from...

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Published inNature immunology Vol. 15; no. 10; pp. 982 - 995
Main Authors Lee, Mike, Kiefel, Helena, LaJevic, Melissa D, Macauley, Matthew S, Kawashima, Hiroto, O'Hara, Edward, Pan, Junliang, Paulson, James C, Butcher, Eugene C
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.10.2014
Nature Publishing Group
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Online AccessGet full text
ISSN1529-2908
1529-2916
1529-2916
DOI10.1038/ni.2983

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Abstract High endothelial vessels (HEVs) provide the conduit for blood-borne leukocytes to enter lymph nodes. Butcher and colleagues report transcriptional profiles of various endothelial cell populations that can explain functional differences of homing-molecule modifications. Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that distinguish HEVs from capillary endothelium and that define tissue-specific HEV specialization. Capillaries expressed gene programs for vascular development. HEV-expressed genes showed enrichment for genes encoding molecules involved in immunological defense and lymphocyte migration. We identify capillary and HEV markers and candidate mechanisms for regulated recruitment of lymphocytes, including a lymph node HEV–selective transmembrane mucin; transcriptional control of functionally specialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for lipid mediators of lymphocyte motility and chemotaxis. We also elucidate a carbohydrate-recognition pathway that targets B cells to intestinal lymphoid tissues, defining CD22 as a lectin-homing receptor for mucosal HEVs.
AbstractList Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that distinguish HEVs from capillary endothelium and that define tissue-specific HEV specialization. Capillaries expressed gene programs for vascular development. HEV-expressed genes showed enrichment for genes encoding molecules involved in immunological defense and lymphocyte migration. We identify capillary and HEV markers and candidate mechanisms for regulated recruitment of lymphocytes, including a lymph node HEV-selective transmembrane mucin; transcriptional control of functionally specialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for lipid mediators of lymphocyte motility and chemotaxis. We also elucidate a carbohydrate-recognition pathway that targets B cells to intestinal lymphoid tissues, defining CD22 as a lectin-homing receptor for mucosal HEVs.
Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that distinguish HEVs from capillary endothelium and that define tissue-specific HEV specialization. Capillaries expressed gene programs for vascular development. HEV-expressed genes showed enrichment for genes encoding molecules involved in immunological defense and lymphocyte migration. We identify capillary and HEV markers and candidate mechanisms for regulated recruitment of lymphocytes, including a lymph node HEV-selective transmembrane mucin; transcriptional control of functionally specialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for lipid mediators of lymphocyte motility and chemotaxis. We also elucidate a carbohydrate-recognition pathway that targets B cells to intestinal lymphoid tissues, defining CD22 as a lectin-homing receptor for mucosal HEVs.Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that distinguish HEVs from capillary endothelium and that define tissue-specific HEV specialization. Capillaries expressed gene programs for vascular development. HEV-expressed genes showed enrichment for genes encoding molecules involved in immunological defense and lymphocyte migration. We identify capillary and HEV markers and candidate mechanisms for regulated recruitment of lymphocytes, including a lymph node HEV-selective transmembrane mucin; transcriptional control of functionally specialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for lipid mediators of lymphocyte motility and chemotaxis. We also elucidate a carbohydrate-recognition pathway that targets B cells to intestinal lymphoid tissues, defining CD22 as a lectin-homing receptor for mucosal HEVs.
Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that distinguish HEVs from capillary endothelium and that define tissue-specific HEV specialization. Capillaries displayed gene programs for vascular development. HEVs were enriched in genes for immune defense and lymphocyte migration. We identify capillary and HEV markers and candidate mechanisms for regulated lymphocyte recruitment including a lymph node HEV-selective transmembrane mucin; transcriptional control of functionally specialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for lipid mediators of lymphocyte motility and chemotaxis. We also elucidate a carbohydrate recognition pathway that targets B cells to intestinal lymphoid tissues, defining CD22 as a lectin-homing receptor for mucosal HEVs.
High endothelial vessels (HEVs) provide the conduit for blood-borne leukocytes to enter lymph nodes. Butcher and colleagues report transcriptional profiles of various endothelial cell populations that can explain functional differences of homing-molecule modifications. Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that distinguish HEVs from capillary endothelium and that define tissue-specific HEV specialization. Capillaries expressed gene programs for vascular development. HEV-expressed genes showed enrichment for genes encoding molecules involved in immunological defense and lymphocyte migration. We identify capillary and HEV markers and candidate mechanisms for regulated recruitment of lymphocytes, including a lymph node HEV–selective transmembrane mucin; transcriptional control of functionally specialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for lipid mediators of lymphocyte motility and chemotaxis. We also elucidate a carbohydrate-recognition pathway that targets B cells to intestinal lymphoid tissues, defining CD22 as a lectin-homing receptor for mucosal HEVs.
Audience Academic
Author Butcher, Eugene C
Paulson, James C
O'Hara, Edward
Macauley, Matthew S
Pan, Junliang
Kawashima, Hiroto
Kiefel, Helena
Lee, Mike
LaJevic, Melissa D
AuthorAffiliation 4 Department of Cell and Molecular Biology, Immunology and Microbial Science, and Chemical Physiology, The Scripps Research Institute, La Jolla, California USA
2 Palo Alto Veterans Institute for Research, Palo Alto, California, USA
5 Department of Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan
1 Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
3 The Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA
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– name: 4 Department of Cell and Molecular Biology, Immunology and Microbial Science, and Chemical Physiology, The Scripps Research Institute, La Jolla, California USA
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  surname: Butcher
  fullname: Butcher, Eugene C
  email: ebutcher@stanford.edu
  organization: Department of Pathology, Laboratory of Immunology and Vascular Biology, Stanford University School of Medicine, Palo Alto Veterans Institute for Research, The Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System
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25232814 - Nat Immunol. 2014 Oct;15(10):906-8. doi: 10.1038/ni.2994
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– reference: JutilaMALy-6C is a monocyte/macrophage and endothelial cell differentiation antigen regulated by interferon-γEur. J. Immunol.198818181918261:CAS:528:DyaL1MXlsFGmtQ%3D%3D284955210.1002/eji.1830181125
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Snippet High endothelial vessels (HEVs) provide the conduit for blood-borne leukocytes to enter lymph nodes. Butcher and colleagues report transcriptional profiles of...
Lymphocytes are recruited from blood by high-endothelial venules (HEVs). We performed transcriptomic analyses and identified molecular signatures that...
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gale
pubmed
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springer
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Enrichment Source
Publisher
StartPage 982
SubjectTerms 13/31
14/19
38
38/39
38/61
631/1647/2017/2079
631/250
631/250/1619/40
631/250/1620
64/60
82/1
82/51
96/34
Animals
Biomedicine
Blood
Capillaries - metabolism
Cell Movement - genetics
Endothelial Cells - metabolism
Endothelium - cytology
Endothelium - metabolism
Female
Flow Cytometry
Gene Expression Profiling
Gene Ontology
Immune response
Immunology
Infectious Diseases
Lymph Nodes - blood supply
Lymphocytes
Lymphocytes - metabolism
Lymphoid Tissue - blood supply
Male
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Microscopy, Confocal
Oligonucleotide Array Sequence Analysis
Properties
Regulation
resource
Tissues
Venules - metabolism
Title Transcriptional programs of lymphoid tissue capillary and high endothelium reveal control mechanisms for lymphocyte homing
URI https://link.springer.com/article/10.1038/ni.2983
https://www.ncbi.nlm.nih.gov/pubmed/25173345
https://www.proquest.com/docview/1657329145
https://www.proquest.com/docview/1563989709
https://www.proquest.com/docview/1664195624
https://pubmed.ncbi.nlm.nih.gov/PMC4222088
Volume 15
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