The “mode” of lymphocyte extravasation through HEV of Peyer's patches and its role in normal homing and inflammation

Azzali, G; Arcari, Maria Luisa; Caldara, Gaetano Felice

doi:10.1016/j.mvr.2007.09.003

Cited by 23 publications

(25 citation statements)

References 52 publications

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“…It is generally assumed that naive lymphocytes move through HEV via a paracellular route through the junctions [22]. Several ultrastructural studies have, however, challenged this concept by suggesting that lymphocytes penetrate HEV via a transcellular route [23,24]. Although our study does not settle this issue, we found that the junctions of HEV are unique due to their lack of immunostaining for vascular claudins including the endothelial cell specific claudin-5 [12].…”

Section: Discussioncontrasting

confidence: 62%

Distinct molecular composition of blood and lymphatic vascular endothelial cell junctions establishes specific functional barriers within the peripheral lymph node

et al. 2008

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Lymph nodes are strategically localized at the interfaces between the blood and lymphatic vascular system, delivering immune cells and antigens to the lymph node. As cellular junctions of endothelial cells actively regulate vascular permeability and cell traffic, we have investigated their molecular composition by performing an extensive immunofluorescence study for adherens and tight junction molecules, including vascular endothelium (VE)-cadherin, the vascular claudins 1, 3, 5 and 12, occludin, members of the junctional adhesion molecule family plus endothelial cell-selective adhesion molecule (ESAM)-1, platelet endothelial cell adhesion molecule-1, ZO-1 and ZO-2. We found that junctions of high endothelial venules (HEV), which serve as entry site for naive lymphocytes, are unique due to their lack of the endothelial cell-specific claudin-5. LYVE-1 + sinus-lining endothelial cells form a diffusion barrier for soluble molecules that arrive at the afferent lymph and use claudin-5 and ESAM-1 to establish characteristic tight junctions. Analysis of the spatial relationship between the different vascular compartments revealed that HEV extend beyond the paracortex into the medullary sinuses, where they are protected from direct contact with the lymph by sinus-lining endothelial cells. The specific molecular architecture of cellular junctions present in blood and lymphatic vessel endothelium in peripheral lymph nodes establishes distinct barriers controlling the distribution of antigens and immune cells within this tissue.

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Section: Discussioncontrasting

confidence: 62%

Distinct molecular composition of blood and lymphatic vascular endothelial cell junctions establishes specific functional barriers within the peripheral lymph node

et al. 2008

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“…Studies of cervical, mesenteric, popliteal, para-aortic, axillary and tibial-popliteal lymph nodes in a range of animal models (rat, mouse, hamster, guinea pig and chicken) have reported predominant use of transcellular diapedesis (Cho and De Bruyn, 1979;Cho and De Bruyn, 1981;Cho and De Bruyn, 1986;Farr and De Bruyn, 1975;Marchesi and Gowans, 1964). Diapedesis in Peyer's patches (in rat, mouse and guinea pig) was seen to occur either by a transcellular pathway exclusively (Azzali et al, 2008;Cho and De Bruyn, 1986) or by concomitant transcellular and paracellular modes (Yamaguchi and Schoefl, 1983). In HEVs of tonsils removed from humans with tonsillitis, HEVs were crossed both paracellularly and transcellularly (Indrasingh et al, 2002).…”

Section: Transcellular Diapedesis In Secondary Lymphoid Organsmentioning

confidence: 99%

“…However, lateral migration also precedes transcellular diapedesis Cinamon et al, 2004;Millan et al, 2006;Yang et al, 2005) and probably has an analogous role in positioning leukocytes optimally (that is, at sites where transcellular pore formation can occur most efficiently). A wide range of in vivo EM studies suggest that transcellular diapedesis occurs preferentially in close juxtaposition to intact intercellular junctions (perijunctionally) (Azzali, 1990;Azzali, 1998;Azzali, 2007a;Azzali and Arcari, 2000;Azzali et al, 2008;Azzali et al, 1990a;Azzali et al, 1990b;Bamforth et al, 1997;Campbell, 1972;Chamberlain and Lichtman, 1978;Cho and De Bruyn, 1981;Cho and De Bruyn, 1986;De Bruyn et al, 1971;Farr et al, 1980;Faustmann and Dermietzel, 1985;Feng et al, 1998;Greenwood et al, 1994;Lossinsky et al, 1989;Lossinsky et al, 1991;Marchesi and Florey, 1960;Marchesi and Gowans, 1964;Wolburg et al, 2005;Wolosewick, 1984) and it has been suggested that leukocytes therefore must somehow 'seek out these regions' (Campbell, 1972). This begs the question of how, in the absence of a discrete preexisting locus (such as endothelial-cell junctions for paracellular diapedesis), such sites for transcellular pore formation (whether perijunctional or otherwise) can be identified by the cell.…”

Section: Lateral Migrationmentioning

confidence: 99%

Mechanisms for transcellular diapedesis: probing and pathfinding by `invadosome-like protrusions'

Carman

2009

Journal of Cell Science

172

171

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Immune-system functions require that blood leukocytes continuously traffic throughout the body and repeatedly cross endothelial barriers (i.e. diapedese) as they enter (intravasate) and exit (extravasate) the circulation. The very earliest studies to characterize diapedesis directly in vivo suggested the coexistence of two distinct migratory pathways of leukocytes: between (paracellular pathway) and directly through (transcellular pathway) individual endothelial cells. In vivo studies over the past 50 years have demonstrated significant use of the transcellular diapedesis pathway in bone marrow, thymus, secondary lymphoid organs, various lymphatic structures and peripheral tissues during inflammation and across the blood-brain barrier and blood-retinal barrier during inflammatory pathology. Recently, the first in vitro reports of transcellular diapedesis have emerged. Together, these in vitro and in vivo observations suggest a model of migratory pathfinding in which dynamic `invadosome-like protrusions' formed by leukocytes have a central role in both identifying and exploiting endothelial locations that are permissive for transcellular diapedesis. Such `probing' activity might have additional roles in this and other settings.

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“…Binding of CCL21 to its receptor CCR7 induces rapid (.1 s) conformational activation of the LFA-1 integrin required for firm arrest of rolling lymphocytes, and it induces over the next tens of seconds to few minutes the acquisition of a polarized phenotype (5)(6)(7). Polarized lymphocytes then crawl in an ICAM-1-dependent manner along the HEV surface prior to transendothelial migration (TEM) through narrow pores of the endothelial barrier and negotiate their passage through the cuff of basement membrane meshworks surrounding fibroblast reticular cells (FRCs) and occasional pericytes (8)(9)(10)(11)(12). FRCs constitute the stromal backbone of the T cell area in the PLN parenchyma and form a three-dimensional (3D) network, which T cells use as contact guidance cues during their scanning of APCs inside the tightly packed lymphoid microenvironment (13).…”

mentioning

confidence: 99%

In Vivo Analysis of Uropod Function during Physiological T Cell Trafficking

Soriano

Hons

Schumann

et al. 2011

The Journal of Immunology

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Migrating lymphocytes acquire a polarized phenotype with a leading and a trailing edge, or uropod. Although in vitro experiments in cell lines or activated primary cell cultures have established that Rho-p160 coiled-coil kinase (ROCK)-myosin II-mediated uropod contractility is required for integrin de-adhesion on two-dimensional surfaces and nuclear propulsion through narrow pores in three-dimensional matrices, less is known about the role of these two events during the recirculation of primary, nonactivated lymphocytes. Using pharmacological antagonists of ROCK and myosin II, we report that inhibition of uropod contractility blocked integrin-independent mouse T cell migration through narrow, but not large, pores in vitro. T cell crawling on chemokine-coated endothelial cells under shear was severely impaired by ROCK inhibition, whereas transendothelial migration was only reduced through endothelial cells with high, but not low, barrier properties. Using three-dimensional thick-tissue imaging and dynamic two-photon microscopy of T cell motility in lymphoid tissue, we demonstrated a significant role for uropod contractility in intraluminal crawling and transendothelial migration through lymph node, but not bone marrow, endothelial cells. Finally, we demonstrated that ICAM-1, but not anatomical constraints or integrin-independent interactions, reduced parenchymal motility of inhibitor-treated T cells within the dense lymphoid microenvironment, thus assigning context-dependent roles for uropod contraction during lymphocyte recirculation.

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The “mode” of lymphocyte extravasation through HEV of Peyer's patches and its role in normal homing and inflammation

Cited by 23 publications

References 52 publications

Distinct molecular composition of blood and lymphatic vascular endothelial cell junctions establishes specific functional barriers within the peripheral lymph node

Distinct molecular composition of blood and lymphatic vascular endothelial cell junctions establishes specific functional barriers within the peripheral lymph node

Mechanisms for transcellular diapedesis: probing and pathfinding by `invadosome-like protrusions'

In Vivo Analysis of Uropod Function during Physiological T Cell Trafficking

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