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 in | Nature immunology Vol. 15; no. 10; pp. 982 - 995 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Nature Publishing Group US
01.10.2014
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 1529-2908 1529-2916 1529-2916 |
DOI | 10.1038/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. |
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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 |
AuthorAffiliation_xml | – name: 2 Palo Alto Veterans Institute for Research, Palo Alto, California, USA – name: 3 The Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA – name: 5 Department of Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan – name: 4 Department of Cell and Molecular Biology, Immunology and Microbial Science, and Chemical Physiology, The Scripps Research Institute, La Jolla, California USA – name: 1 Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA |
Author_xml | – sequence: 1 givenname: Mike surname: Lee fullname: Lee, Mike organization: Department of Pathology, Laboratory of Immunology and Vascular Biology, Stanford University School of Medicine – sequence: 2 givenname: Helena surname: Kiefel fullname: Kiefel, Helena organization: Department of Pathology, Laboratory of Immunology and Vascular Biology, Stanford University School of Medicine – sequence: 3 givenname: Melissa D surname: LaJevic fullname: LaJevic, Melissa D organization: Department of Pathology, Laboratory of Immunology and Vascular Biology, Stanford University School of Medicine – sequence: 4 givenname: Matthew S surname: Macauley fullname: Macauley, Matthew S organization: Departments of Cell and Molecular Biology, Immunology and Microbial Science, and Chemical Physiology, The Scripps Research Institute – sequence: 5 givenname: Hiroto surname: Kawashima fullname: Kawashima, Hiroto organization: Department of Biochemistry, School of Pharmacy and Pharmaceutical Sciences – sequence: 6 givenname: Edward surname: O'Hara fullname: O'Hara, Edward organization: Palo Alto Veterans Institute for Research – sequence: 7 givenname: Junliang surname: Pan fullname: Pan, Junliang organization: Palo Alto Veterans Institute for Research – sequence: 8 givenname: James C surname: Paulson fullname: Paulson, James C organization: Departments of Cell and Molecular Biology, Immunology and Microbial Science, and Chemical Physiology, The Scripps Research Institute – sequence: 9 givenname: Eugene C 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 |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25173345$$D View this record in MEDLINE/PubMed |
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PublicationPlace | New York |
PublicationPlace_xml | – name: New York – name: United States |
PublicationTitle | Nature immunology |
PublicationTitleAbbrev | Nat Immunol |
PublicationTitleAlternate | Nat Immunol |
PublicationYear | 2014 |
Publisher | Nature Publishing Group US Nature Publishing Group |
Publisher_xml | – name: Nature Publishing Group US – name: Nature Publishing Group |
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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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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 |
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