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Nat Immunol. 2014 Oct;15(10):982-95. doi: 10.1038/ni.2983. Epub 2014 Aug 31.

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

Author information

1
Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
2
Departments of Cell and Molecular Biology, Immunology and Microbial Science, and Chemical Physiology, The Scripps Research Institute, La Jolla, California USA.
3
Palo Alto Veterans Institute for Research, Palo Alto, California, USA.
4
1] Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA. [2] Palo Alto Veterans Institute for Research, Palo Alto, California, USA. [3] The Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, USA.

Erratum in

  • Nat Immunol. 2015 Feb;16(2):214. Kawashima, Hiroto [added].

Abstract

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.

PMID:
25173345
PMCID:
PMC4222088
DOI:
10.1038/ni.2983
[Indexed for MEDLINE]
Free PMC Article

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