l-Selectin – A dynamic regulator of leukocyte migration

Wedepohl, Stefanie; Beceren‐Braun, Figen; Riese, Sebastian B.; Buscher, Konrad; Enders, Sven; Bernhard, Gesche; Kilian, Karin; Blanchard, Véronique; Dernedde, Jens; Tauber, Rudolf

doi:10.1016/j.ejcb.2011.02.007

Cited by 64 publications

(54 citation statements)

References 102 publications

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“…Selectin L was not expressed by skin DCs, consistent with an essential role in blood leukocyte emigration through vascular endothelium (50). Presence or absence of some markers were specific for skin DC subpopulations.…”

Section: Discussionmentioning

confidence: 78%

Identification of Lineage Relationships and Novel Markers of Blood and Skin Human Dendritic Cells

Harman

Bye

Nasr

et al. 2013

The Journal of Immunology

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The lineage relationships and fate of human dendritic cells (DCs) have significance for a number of diseases including HIV where both blood and tissue DCs may be infected. We used gene expression profiling of human monocyte and DC subpopulations sorted directly from blood and skin to define the lineage relationships. We also compared these with monocyte-derived DCs (MDDCs) and MUTZ3 Langerhans cells (LCs) to investigate their relevance as model skin DCs. Hierarchical clustering analysis showed that myeloid DCs clustered according to anatomical origin rather than putative lineage. Plasmacytoid DCs formed the most discrete cluster, but ex vivo myeloid cells formed separate clusters of cells both in blood and in skin. Separate and specific DC populations could be determined within skin, and the proportion of CD14+ dermal DCs (DDCs) was reduced and CD1a+ DDCs increased during culture, suggesting conversion to CD1a+-expressing cells in situ. This is consistent with origin of the CD1a+ DDCs from a local precursor rather than directly from circulating blood DCs or monocyte precursors. Consistent with their use as model skin DCs, the in vitro–derived MDDC and MUTZ3 LC populations grouped within the skin DC cluster. MDDCs clustered most closely to CD14+ DDCs; furthermore, common unique patterns of C-type lectin receptor expression were identified between these two cell types. MUTZ3 LCs, however, did not cluster closely with ex vivo–derived LCs. We identified differential expression of novel genes in monocyte and DC subsets including genes related to DC surface receptors (including C-type lectin receptors, TLRs, and galectins).

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Section: Discussionmentioning

confidence: 78%

Identification of Lineage Relationships and Novel Markers of Blood and Skin Human Dendritic Cells

Harman

Bye

Nasr

et al. 2013

The Journal of Immunology

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“…The disparity may reflect differences in the population-specific genetic determinants 33 and the case and control recruitment criteria of the respective studies. Of interest, the identification of SELL, encoding the leukocyte migration protein selectin L 34 ARTICLE processes. Both systems are thought to be critical in acne pathophysiology 25,35 .…”

Section: Discussionmentioning

confidence: 99%

“…We thank Saxena Alka (London, UK); Ulrike Blume-Peytavi (Berlin, Germany); Leaca Crawford 34 ; Jana Estafan 24 …”

Section: Acknowledgementsmentioning

confidence: 99%

Genome-wide association study identifies three novel susceptibility loci for severe Acne vulgaris

et al. 2014

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“…Engagement of CD62L supports the capture of T lymphocytes from the bloodstream, followed by their rolling along HEVs. Upon binding its ligands, CD62L also initiates a number of events, including activation of signaling cascades, rearrangement of the actin cytoskeleton, and enhancement of integrin binding to components of the extracellular matrix expressed by HEVs, which is a prerequisite for T cell arrest and transmigration (4). In addition, CD62L cross talks with the T cell receptor (TCR), since triggering of CD62L provides a costimulatory signal for lymphocyte activation via the TCR (5) and TCR activation enhances the binding activity of CD62L (6).…”

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confidence: 99%

HIV-1 Nef and Vpu Interfere with L-Selectin (CD62L) Cell Surface Expression To Inhibit Adhesion and Signaling in Infected CD4⁺T Lymphocytes

Vassena

Giuliani

Koppensteiner

et al. 2015

J Virol

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Leukocyte recirculation between blood and lymphoid tissues is required for the generation and maintenance of immune responses against pathogens and is crucially controlled by the L-selectin (CD62L) leukocyte homing receptor. CD62L has adhesion and signaling functions and initiates the capture and rolling on the vascular endothelium of cells entering peripheral lymph nodes. This study reveals that CD62L is strongly downregulated on primary CD4؉ T lymphocytes upon infection with human immunodeficiency virus type 1 (HIV-1). Reduced cell surface CD62L expression was attributable to the Nef and Vpu viral proteins and not due to increased shedding via matrix metalloproteases. Both Nef and Vpu associated with and sequestered CD62L in perinuclear compartments, thereby impeding CD62L transport to the plasma membrane. In addition, Nef decreased total CD62L protein levels. Importantly, infection with wild-type, but not Nef-and Vpu-deficient, HIV-1 inhibited the capacity of primary CD4؉ T lymphocytes to adhere to immobilized fibronectin in response to CD62L ligation. Moreover, HIV-1 infection impaired the signaling pathways and costimulatory signals triggered in primary CD4؉ T cells by CD62L ligation. We propose that HIV-1 dysregulates CD62L expression to interfere with the trafficking and activation of infected T cells. Altogether, this novel HIV-1 function could contribute to virus dissemination and evasion of host immune responses. Effective immune surveillance is dependent on the constitutive recirculation of lymphocytes through anatomically dispersed secondary organs. To gain entry to the peripheral lymph nodes (PLNs), lymphocytes must bind and traverse high endothelial venules (HEVs) through a multistep process that is initiated by the interaction of the lectin-like receptor L-selectin (CD62L) on the surfaces of lymphocytes with glycoproteins expressed by HEVs (e.g., CD34 and GlyCAM-1) (1). CD62L knockout mouse models demonstrated that CD62L plays an essential role in leukocyte homing to lymphoid tissues and sites of inflammation (2), as well as in the generation of T cell responses (3). Engagement of CD62L supports the capture of T lymphocytes from the bloodstream, followed by their rolling along HEVs. Upon binding its ligands, CD62L also initiates a number of events, including activation of signaling cascades, rearrangement of the actin cytoskeleton, and enhancement of integrin binding to components of the extracellular matrix expressed by HEVs, which is a prerequisite for T cell arrest and transmigration (4). In addition, CD62L cross talks with the T cell receptor (TCR), since triggering of CD62L provides a costimulatory signal for lymphocyte activation via the TCR (5) and TCR activation enhances the binding activity of CD62L (6).Upon antigen (Ag) stimulation of T cells, the ectodomain of CD62L is cleaved by activated matrix metalloproteases (MMPs) and released in a soluble form (sCD62L), thus allowing reentry into circulation of T cells with helper and effector functions (7). Shedding of CD62L has importa...

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l-Selectin – A dynamic regulator of leukocyte migration

Cited by 64 publications

References 102 publications

Identification of Lineage Relationships and Novel Markers of Blood and Skin Human Dendritic Cells

Identification of Lineage Relationships and Novel Markers of Blood and Skin Human Dendritic Cells

Genome-wide association study identifies three novel susceptibility loci for severe Acne vulgaris

HIV-1 Nef and Vpu Interfere with L-Selectin (CD62L) Cell Surface Expression To Inhibit Adhesion and Signaling in Infected CD4⁺T Lymphocytes

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l-Selectin – A dynamic regulator of leukocyte migration

Cited by 64 publications

References 102 publications

Identification of Lineage Relationships and Novel Markers of Blood and Skin Human Dendritic Cells

Identification of Lineage Relationships and Novel Markers of Blood and Skin Human Dendritic Cells

Genome-wide association study identifies three novel susceptibility loci for severe Acne vulgaris

HIV-1 Nef and Vpu Interfere with L-Selectin (CD62L) Cell Surface Expression To Inhibit Adhesion and Signaling in Infected CD4+T Lymphocytes

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HIV-1 Nef and Vpu Interfere with L-Selectin (CD62L) Cell Surface Expression To Inhibit Adhesion and Signaling in Infected CD4⁺T Lymphocytes