scholarly journals Significant decrease in α1,3-linked fucose in association with increase in 6-sulfated N-acetylglucosamine in peripheral lymph node addressin of FucT-VII-deficient mice exhibiting diminished lymphocyte homing

Glycobiology ◽  
2006 ◽  
Vol 17 (3) ◽  
pp. 277-293 ◽  
Author(s):  
Nobuyoshi Hiraoka ◽  
Bronislawa Petryniak ◽  
Hiroto Kawashima ◽  
Junya Mitoma ◽  
Tomoya O Akama ◽  
...  
Keyword(s):  
Lymph Node ◽  
Peripheral Lymph Node ◽  
Lymphocyte Homing ◽  
Peripheral Lymph ◽  
Deficient Mice

scholarly journals Immunohistologic and functional characterization of a vascular addressin involved in lymphocyte homing into peripheral lymph nodes.

1988 ◽  
Vol 107 (5) ◽  
pp. 1853-1862 ◽  
Author(s):  
P R Streeter ◽  
B T Rouse ◽  
E C Butcher
Keyword(s):  
Endothelial Cells ◽  
Lymph Node ◽  
Lymph Nodes ◽  
Peyer's Patches ◽  
Peripheral Lymph Node ◽  
Lymphocyte Homing ◽  
Tissue Specific ◽  
Peripheral Lymph

The tissue localization or "homing" of circulating lymphocytes is directed in part by specialized vessels that define sites of lymphocyte exit from the blood. In peripheral lymph nodes, mucosal lymphoid tissues (Peyer's patches and appendix), and sites of chronic inflammation, for example, lymphocytes leave the blood by adhering to and migrating between those endothelial cells lining postcapillary high endothelial venules (HEV). Functional analyses of lymphocyte interactions with HEV have shown the lymphocytes can discriminate between HEV in different tissues, indicating that HEV express tissue-specific determinants or address signals for lymphocyte recognition. We recently described such a tissue-specific "vascular addressin" that is selectively expressed by endothelial cells supporting lymphocyte extravasation into mucosal tissues and that appears to be required for mucosa-specific lymphocyte homing (Streeter, P. R., E. L. Berg, B. N. Rouse, R. F. Bargatze, and E. C. Butcher. 1988. Nature (Lond.). 331:41-46). Here we document the existence and tissue-specific distribution of a distinct HEV differentiation antigen. Defined by monoclonal antibody MECA-79, this antigen is expressed at high levels on the lumenal surface and in the cytoplasm of HEV in peripheral lymph nodes. By contrast, although MECA-79 stains many HEV in the mucosal Peyer's patches, expression in most cases is restricted to the perivascular or ablumenal aspect of these venules. In the small intestine lamina propria, a mucosa-associated site that supports the extravasation of lymphocytes, venules do not stain with MECA-79. Finally, we demonstrate that MECA-79 blocks binding of both normal lymphocytes and a peripheral lymph node-specific lymphoma to peripheral lymph node HEV in vitro and that it also inhibits normal lymphocyte homing to peripheral lymph nodes in vivo without significantly influencing lymphocyte interactions with Peyer's patch HEV in vitro or in vivo. Thus, MECA-79 defines a novel vascular addressin involved in directing lymphocyte homing to peripheral lymph nodes.

scholarly journals Identification of a carbohydrate-based endothelial ligand for a lymphocyte homing receptor.

1991 ◽  
Vol 113 (5) ◽  
pp. 1213-1221 ◽  
Author(s):  
Y Imai ◽  
M S Singer ◽  
C Fennie ◽  
L A Lasky ◽  
S D Rosen
Keyword(s):  
Lymph Node ◽  
Peripheral Lymph Node ◽  
Lymphocyte Homing ◽  
High Endothelial Venules ◽  
Homing Receptor ◽  
Calcium Dependent ◽  
Lymph Node Homing ◽  
Recombinant Receptor ◽  
Peripheral Lymph ◽  
Mouse Lymphocytes

Lymphocyte attachment to high endothelial venules within lymph nodes is mediated by the peripheral lymph node homing receptor (pnHR), originally defined on mouse lymphocytes by the MEL-14 mAb. The pnHR is a calcium-dependent lectin-like receptor, a member of the LEC-CAM family of adhesion proteins. Here, using a soluble recombinant form of the homing receptor, we have identified an endothelial ligand for the pnHR as an approximately 50-kD sulfated, fucosylated, and sialylated glycoprotein, which we designate Sgp50 (sulfated glycoprotein of 50 kD). Recombinant receptor binding to this lymph node-specific glycoprotein requires calcium and is inhibitable by specific carbohydrates and by MEL-14 mAb. Sialylation of the component is required for binding. Additionally, the glycoprotein is precipitated by MECA-79, an adhesion-blocking mAb reactive with lymph node HEV. A related glycoprotein of approximately 90 kD (designated as Sgp90) is also identified.

scholarly journals The human peripheral lymph node vascular addressin is a ligand for LECAM-1, the peripheral lymph node homing receptor.

1991 ◽  
Vol 114 (2) ◽  
pp. 343-349 ◽  
Author(s):  
E L Berg ◽  
M K Robinson ◽  
R A Warnock ◽  
E C Butcher
Keyword(s):  
Lymph Node ◽  
Lymphoid Tissues ◽  
Dependent Manner ◽  
Peripheral Lymph Node ◽  
Lymphocyte Homing ◽  
High Endothelial Venules ◽  
Homing Receptor ◽  
Calcium Dependent ◽  
Lymph Node Homing ◽  
Peripheral Lymph

The trafficking of lymphocytes from the blood and into lymphoid organs is controlled by tissue-selective lymphocyte interactions with specialized endothelial cells lining post capillary venules, in particular the high endothelial venules (HEV) found in lymphoid tissues and sites of chronic inflammation. Lymphocyte interactions with HEV are mediated in part by lymphocyte homing receptors and tissue-specific HEV determinants, the vascular addressins. A peripheral lymph node addressin (PNAd) has been detected immunohistologically in mouse and man by monoclonal antibody MECA-79, which inhibits lymphocyte homing to lymph nodes and lymphocyte binding to lymph node and tonsillar HEV. The human MECA-79 antigen, PNAd, is molecularly distinct from the 65-kD mucosal vascular addressin. The most abundant iodinated species by SDS-PAGE is 105 kD. When affinity isolated and immobilized on glass slides, MECA-79 immunoisolated material binds human and mouse lymphocytes avidly in a calcium dependent manner. Binding is blocked by mAb MECA-79, by antibodies against mouse or human LECAM-1 (the peripheral lymph node homing receptor, the MEL-14 antigen, LAM-1), and by treatment of PNAd with neuraminidase. Expression of LECAM-1 cDNA confers PNAd binding ability on a transfected B cell line. We conclude that LECAM-1 mediates lymphocyte binding to PNAd, an interaction that involves the lectin activity of LECAM-1 and carbohydrate determinants on the addressin.

scholarly journals The influence of afferent lymphatic vessel interruption on vascular addressin expression.

1991 ◽  
Vol 115 (1) ◽  
pp. 85-95 ◽  
Author(s):  
R E Mebius ◽  
P R Streeter ◽  
J Brevé ◽  
A M Duijvestijn ◽  
G Kraal
Keyword(s):  
Lymph Node ◽  
Lymph Nodes ◽  
Lymphatic Vessel ◽  
Lymphatic Vessels ◽  
Lymphoid Tissues ◽  
Peripheral Lymph Node ◽  
Lymphocyte Homing ◽  
High Endothelial Venules ◽  
Peripheral Lymph

Tissue-selective lymphocyte homing is directed in part by specialized vessels that define sites of lymphocyte exit from the blood. These vessels, the post capillary high endothelial venules (HEV), are found in organized lymphoid tissues, and at sites of chronic inflammation. Lymphocytes bearing specific receptors, called homing receptors, recognize and adhere to their putative ligands on high endothelial cells, the vascular addressins. After adhesion, lymphocytes enter organized lymphoid tissues by migrating through the endothelial cell wall. Cells and/or soluble factors arriving in lymph nodes by way of the afferent lymph supply have been implicated in the maintenance of HEV morphology and efficient lymphocyte homing. In the study reported here, we assessed the influence of afferent lymphatic vessel interruption on lymph node composition, organization of cellular elements; and on expression of vascular addressins. At 1 wk after occlusion of afferent lymphatic vessels, HEV became flat walled and expression of the peripheral lymph node addressin disappeared from the luminal aspect of most vessels, while being retained on the abluminal side. In addition, an HEV-specific differentiation marker, defined by mAb MECA-325, was undetectable at 7-d postocclusion. In vivo homing studies revealed that these modified vessels support minimal lymphocyte traffic from the blood. After occlusion, we observed dramatic changes in lymphocyte populations and at 7-d postsurgery, lymph nodes were populated predominantly by cells lacking the peripheral lymph node homing receptor LECAM-1. In addition, effects on nonlymphoid cells were observed: subcapsular sinus macrophages, defined by mAb MOMA-1, disappeared; and interdigitating dendritic cells, defined by mAb NLDC-145, were dramatically reduced. These data reveal that functioning afferent lymphatics are centrally involved in maintaining normal lymph node homeostasis.

scholarly journals Evolutionary conservation of tissue-specific lymphocyte-endothelial cell recognition mechanisms involved in lymphocyte homing.

1988 ◽  
Vol 107 (5) ◽  
pp. 1845-1851 ◽  
Author(s):  
N W Wu ◽  
S Jalkanen ◽  
P R Streeter ◽  
E C Butcher
Keyword(s):  
Lymph Node ◽  
Endothelial Cell ◽  
Human Lymphocytes ◽  
Lymphoid Tissues ◽  
Cell Recognition ◽  
Peripheral Lymph Node ◽  
Lymphocyte Homing ◽  
Tissue Specific ◽  
Peripheral Lymph ◽  
Organ Specific

Tissue-specific interactions with specialized high endothelial venules (HEV) direct the homing of lymphocytes from the blood into peripheral lymph nodes, mucosal lymphoid organs, and tissue sites of chronic inflammation. These interactions have been demonstrated in all mammalian species examined and thus appear highly conserved. To assess the degree of evolutionary divergence in lymphocyte-HEV recognition mechanisms, we have studied the ability of lymphocytes to interact with HEV across species barriers. By using an in vitro assay of lymphocyte binding to HEV in frozen sections of lymphoid tissues, we confirm that mouse, guinea pig, and human lymphocytes bind to xenogeneic as well as homologous HEV. In addition, we show that mouse and human lymphoid cell lines that bind selectively to either peripheral lymph node or mucosal vessels (Peyer's patches, appendix) in homologous lymphoid tissues exhibit the same organ specificity in binding to xenogeneic HEV. Furthermore, monoclonal antibodies that recognize lymphocyte "homing receptors" and block homologous lymphocyte binding to peripheral lymph node or to mucosal HEV, also inhibit lymphocyte interactions with xenogeneic HEV in a tissue-specific fashion. Similarly, anti-HEV antibodies against organ-specific mouse high endothelial cell "addressins" involved in lymphocyte homing to peripheral lymph node or mucosal lymphoid organs, not only block the adhesion of mouse lymphocytes but also of human lymphocytes to target mouse HEV. The results illustrate a remarkable degree of functional conservation of elements mediating these cell-cell recognition events involved in organ-specific lymphocyte homing.

scholarly journals Characterization of a human homologue of the murine peripheral lymph node homing receptor.

1989 ◽  
Vol 109 (1) ◽  
pp. 421-427 ◽  
Author(s):  
B R Bowen ◽  
T Nguyen ◽  
L A Lasky
Keyword(s):  
Cell Adhesion ◽  
Lymph Node ◽  
Adhesion Molecule ◽  
Carbohydrate Binding ◽  
Human Homologue ◽  
Peripheral Lymph Node ◽  
Homing Receptor ◽  
Lymph Node Homing ◽  
Peripheral Lymph ◽  
Human Receptor

Lymphocyte trafficking is a fundamental aspect of the immune system that allows B and T lymphocytes with diverse antigen recognition specificities to be exposed to various antigenic stimuli in spatially distinct regions of an organism. A lymphocyte adhesion molecule that is involved with this trafficking phenomenon has been termed the homing receptor. Previous work (Lasky, L., T. Yednock, M. Singer, D. Dowbenko, C. Fennie, H. Rodriguez, T. Nguyen, S. Stachel, and S. Rosen. 1989. Cell. 56:1045-1055) has characterized a cDNA clone encoding a murine homing receptor that is involved in trafficking of lymphocytes to peripheral lymph nodes. This molecule was found to contain a number of protein motifs, the most intriguing of which was a carbohydrate binding domain, or lectin, that is apparently involved in the adhesive interaction between murine lymphocytes and peripheral lymph node endothelium. In this study, we have used the murine cDNA clone to isolate a human homologue of this peripheral lymph node-specific adhesion molecule. The human receptor was found to be highly homologous to the murine receptor in overall sequence, but showed no sequence similarity to another surface protein that may be involved with human lymphocyte homing, the Hermes glycoprotein. The extracellular region of the human receptor contained an NH2 terminally located carbohydrate binding domain followed by an EGF-like domain and a domain containing two repeats of a complement binding motif. Transient cell transfection assays using the human receptor cDNA showed that it encoded a surface glycoprotein that cross reacted with a polyclonal antibody directed against the murine peripheral lymph node homing receptor. Interestingly, the human receptor showed a high degree of sequence homology to another human cell adhesion glycoprotein, the endothelial cell adhesion molecule ELAM.

scholarly journals Epidemiology of Peripheral Lymph Node Tuberculosis and Genotyping of M. tuberculosis Strains: A Case-Control Study

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0132400 ◽  
Author(s):  
Chinmay Khandkar ◽  
Zinta Harrington ◽  
Peter J. Jelfs ◽  
Vitali Sintchenko ◽  
Claudia C. Dobler
Keyword(s):  
Lymph Node ◽  
Case Control Study ◽  
Case Control ◽  
Peripheral Lymph Node ◽  
Peripheral Lymph ◽  
Lymph Node Tuberculosis ◽  
Control Study

scholarly journals Demonstration that a lectin-like receptor (gp90MEL) directly mediates adhesion of lymphocytes to high endothelial venules of lymph nodes.

1989 ◽  
Vol 109 (5) ◽  
pp. 2463-2469 ◽  
Author(s):  
J S Geoffroy ◽  
S D Rosen
Keyword(s):  
Lymph Node ◽  
Lymphoid Organ ◽  
Lymphoid Organs ◽  
Surface Glycoprotein ◽  
Lymphocyte Migration ◽  
Peripheral Lymph Node ◽  
Adhesive Interaction ◽  
High Endothelial Venules ◽  
Cell Surface Glycoprotein ◽  
Peripheral Lymph

Lymphocyte migration from the blood into most secondary lymphoid organs is initiated by a highly selective adhesive interaction with the endothelium of specialized blood vessels known as high endothelial venules (HEV). The propensity of lymphocytes to migrate to particular lymphoid organs is known as lymphocyte homing, and the receptors on lymphocytes that dictate interactions with HEV at particular anatomical sites are designated "homing receptors". Based upon antibody blockade experiments and cell-type distribution studies, a prominent candidate for the peripheral lymph node homing receptor in mouse is the approximately 90-kD cell surface glycoprotein (gp90MEL) recognized by the monoclonal antibody MEL-14. Previous work, including sequencing of a cDNA encoding for this molecule, supports the possibility that gp90MEL is a calcium-dependent lectin-like receptor. Here, we show that immunoaffinity-purified gp90MEL interacts in a sugar-inhibitable manner with sites on peripheral lymph node HEV and prevents attachment of lymphocytes. Lymphocyte attachment to HEV in Peyer's patches, a gut-associated lymphoid organ, is not affected by gp90MEL. The results demonstrate that gp90MEL, as a lectin-like receptor, directly bridges lymphocytes to the endothelium.

Peripheral Lymph Node Recurrence of Tuberculosis After Ustekinumab Treatment

2012 ◽  
Vol 148 (11) ◽  
pp. 1332 ◽  
Author(s):  
Ana I. Sánchez-Moya ◽  
Esteban Daudén
Keyword(s):  
Lymph Node ◽  
Peripheral Lymph Node ◽  
Lymph Node Recurrence ◽  
Peripheral Lymph
Sign in / Sign up

Export Citation Format

Share Document