The S1P-analog FTY720 differentially modulates T-cell homing via HEV: T-cell–expressed S1P1 amplifies integrin activation in peripheral lymph nodes but not in Peyer patches

Halin, Cornelia; Scimone, M. Lucila; Bonasio, Roberto; Gauguet, Jean-Marc; Mempel, Thorsten R.; Quackenbush, Elizabeth J.; Proia, Richard L.; Mandala, Suzanne; Andrian, Ulrich H. von

doi:10.1182/blood-2004-09-3687

Cited by 108 publications

(96 citation statements)

References 44 publications

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“…Because the majority of naive T cells show little in vitro response to ligands for the other defined chemokine receptors, these observations suggest that additional, still-to-be-characterized Gi-coupled receptors are involved in promoting T cell motility within lymphoid organs. Sphingosine-1-phosphate receptor 1 is expressed on naive T cells, but the ligand sphingosine-1-phosphate is present in only low amounts in LNs (14,35), and in studies where sphingosine-1-phosphate receptor function was modulated using agonists or antagonists, there were no effects on T cell motility in the T zone (36,37).…”

Section: Discussionmentioning

confidence: 99%

CC Chemokine Receptor 7 Contributes to Gi-Dependent T Cell Motility in the Lymph Node

Okada

Cyster

2007

The Journal of Immunology

175

169

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Naive T cells migrate extensively within lymph node (LN) T zones to scan for Ag-bearing dendritic cells. However, the extracellular signals controlling T cell motility in LNs are not well defined. In this study, by real-time imaging of LNs, we show that the inhibition of Gi signaling in T cells severely impairs their migration. The chemokine CCL21, a ligand of CCR7, strongly induces chemokinesis in vitro, and T cell motility in LNs from CCR7 ligand-deficient plt/plt mice was reduced. CCR7-deficient T cells in wild-type LNs showed a similar reduction in motility, and antagonism of CXCR4 function did not further decrease their motility. The effect of CCR7 or CCR7-ligand deficiency could account for ∼40% of the Gi-dependent motility. These results reveal a role for CCR7 in promoting T cell migration within lymphoid organ T zones, and they suggest the additional involvement of novel Gi-coupled receptors in promoting T cell motility at these sites.

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Section: Discussionmentioning

confidence: 99%

CC Chemokine Receptor 7 Contributes to Gi-Dependent T Cell Motility in the Lymph Node

Okada

Cyster

2007

The Journal of Immunology

175

169

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“…However, the physiological paucity of circulating CLP-2 may not necessarily reflect an inability to leave the BM; a depletion of bloodborne leukocytes could also result from their rapid clearance in a target tissue. A case in point are naïve T cells, which are abundant in blood as they recirculate between blood and lymphoid organs but rapidly disappear from the circulation when they are prevented from leaving lymphoid tissues after homing (45). Based on published data (45), we calculate the hourly rate at which naïve T cells home to peripheral lymph nodes after i.…”

Section: Discussionmentioning

confidence: 99%

A multistep adhesion cascade for lymphoid progenitor cell homing to the thymus

Scimone

Aifantis

Apostolou

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

139

180

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Homing of bone marrow (BM)-derived progenitors to the thymus is essential for T cell development. We have previously reported that two subpopulations of common lymphoid progenitors, CLP-1 and CLP-2, coexist in the BM and give rise to lymphocytes. We demonstrate that CLP-2 migrate to the thymus more efficiently than any other BM-derived progenitors. Short-term adoptive transfer experiments revealed that CLP-2 homing involves P-selectin͞ P-selectin glycoprotein ligand 1 interactions, pertussis toxin-sensitive chemoattractant signaling by CC chemokine ligand 25 through CC chemokine receptor 9, and binding of the integrins ␣4␤1 and ␣L␤2 to their respective ligands, vascular cell adhesion molecule 1 and intercellular adhesion molecule 1. Preferential thymus-tropism of CLP-2 correlated with higher chemokine receptor 9 expression than on other BM progenitors. Thus, CLP access to the thymus is controlled by a tissue-specific and subset-selective multistep adhesion cascade.cell trafficking ͉ chemokines ͉ integrin ͉ lymphopoiesis ͉ selectin

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“…1A). At this time point, entry from the peripheral blood into LNs directly determined the CD45.1 cell numbers within recipient LNs (17).…”

Section: Adoptive Cell Transfersmentioning

confidence: 99%

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

Tan

Yeo

Wong

et al. 2012

The Journal of Immunology

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During inflammation, accumulation of immune cells in activated lymph nodes (LNs), coupled with a transient shutdown in lymphocyte exit, results in dramatic cellular expansion. Counter-regulatory measures to restrain LN expansion must exist and may include re-establishment of lymphocyte egress to steady-state levels. Indeed, we show in a murine model that egress of lymphocytes from LNs was returned to steady-state levels during prolonged inflammation following initial retention. This restoration in lymphocyte egress was supported by a preferential expansion of cortical and medullary sinuses during late inflammation. Cortical and medullary sinus remodeling during late inflammation was dependent on temporal and spatial changes in vascular endothelial growth factor-A distribution. Specifically, its expression was restricted to the subcapsular space of the LN during early inflammation, whereas its expression was concentrated in the paracortical and medullary regions of the LN at later stages. We next showed that this process was mostly driven by the synergistic cross-talk between fibroblastic reticular cells and interstitial flow. Our data shed new light on the biological significance of LN lymphangiogenesis during prolonged inflammation and further underscore the collaborative roles of stromal cells, immune cells, and interstitial flow in modulating LN plasticity and function.

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The S1P-analog FTY720 differentially modulates T-cell homing via HEV: T-cell–expressed S1P1 amplifies integrin activation in peripheral lymph nodes but not in Peyer patches

Cited by 108 publications

References 44 publications

CC Chemokine Receptor 7 Contributes to Gi-Dependent T Cell Motility in the Lymph Node

CC Chemokine Receptor 7 Contributes to Gi-Dependent T Cell Motility in the Lymph Node

A multistep adhesion cascade for lymphoid progenitor cell homing to the thymus

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

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