Syndecan-3 is a dendritic cell-specific attachment receptor for HIV-1

Witte, Lot de; Bobardt, Michael; Chatterji, Udayan; Degeest, Gisèle; Gourichon, David; Geijtenbeek, Teunis B. H.; Gallay, Philippe

doi:10.1073/pnas.0703747104

Cited by 139 publications

(121 citation statements)

References 49 publications

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“…Although similar mechanisms were assumed to be involved in LC transmission of HIV-1, it is becoming evident that LC might have a more complicated role in transmission [25]. Monocyte-derived DC capture HIV through the CLR DC-SIGN [26] and, to lesser degrees, mannose receptor and heparin sulphate proteoglycan syndecan-3 [27]. HIV-1 is either endocytosed or transferred directly to CD4 and CCR5 resulting in viral-cell membrane fusion and infection.…”

Section: Subsets In Hiv-1 Transmissionmentioning

confidence: 99%

“…These data imply that immature DC and LC in contrast to their mature forms are more important in HIV-1 transmission. Viral endocytosis leads to partial acid-proteolytic degradation in the late endosome, although some virus may be retained in its infectious state for longer periods [27,28] [26]. However, HIV entry via fusion leads to de novo productive infection first detectable at 24 h and with a plateau in vitro at 72 h. Recent studies suggest this de novo produced virus can re-enter the same or adjacent DC by endocytosis and the latter can also be infected de novo, thus mixing up the initial two distinct phases of viral endocytic degradation and de novo infection.…”

Section: Subsets In Hiv-1 Transmissionmentioning

confidence: 99%

Section: Subsets In Hiv-1 Transmissionmentioning

confidence: 99%

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Langerhans cells and viral immunity

2008

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Langerhans cells (LC) are a unique dendritic cell subset that are located in mucosal stratified squamous epithelium and skin epidermis. Their location is ideally suited for their function as antigen presenting cells that capture invading viruses and induce anti-viral immunity. However, it is becoming evident that the interaction between LC and viruses can result in different responses, depending on the virus and the receptors involved. Here we will discuss the recent data on the similarities and differences in roles of LC in viral immunity to and infection with HIV, herpes simplex and varicella-zoster virus. Although all three viruses interact with LC during initial infection, the effects can be quite different, reflecting differences in biology and pathogenesis. Key words: Dendritic cells Á Langerhans cells Á Infectious diseases Á HIV Á HerpesvirusesSee accompanying mini-review by Kaplan et al. Biology of LC and interactions with virusesThe resident epidermal dendritic cells (DC), Langerhans cells (LC), form a tight network with each other and with the surrounding keratinocytes via E-cadherin in the skin or mucosal stratified squamous epithelium. In the anogenital region they are distributed throughout the anogenital skin and mucosa including vagina, ectocervix as well as male foreskin. In stratified squamous epithelium, LC overlie interstitial or dermal DC [1]. LC can repopulate from local and blood-borne precursors (reviewed by Kaplan et al. in this issue [2]). Similar to other myeloid DC, LC are able to bridge innate and adaptive immunity. They are able to interact directly with microorganisms at the periphery to produce effector cytokines and initiate or restimulate activation of T and B lymphocytes through antigen presentation. LC express different pattern recognition receptors such as C-type lectin receptors (CLR) and Toll-like receptors (TLR), to bind and capture pathogens. These interactions result in activation of intracellular signalling pathways leading to LC activation and cytokine induction. The CLR expressed by skin DC differ by site: Langerin by epidermal LC and DC-SIGN and mannose receptor by dermal DC. LC like other migratory DC are in an immature, highly endocytic state while sessile in the skin/mucosa. However after pathogen binding to TLR and uptake, LC become mature and migratory, downregulating their endocytic and antigen processing capacity. Mature LC migrate to the lymph nodes where they are directly or indirectly involved in presentation of pathogenderived antigens on MHC Class I and II to T cells, resulting in activation of antigen-specific T cells [2][3][4]. Recent studies have raised the possibility that LC may have an immunosuppressive role [5][6][7]. Kaplan et al. [2] showed that contact hypersensitivity was amplified on LC ablation, while Cumberbatch et al.[5] found defective LC mobilisation in patients with psoriasis. Immunosuppression rather than stimulation could be explained, in part, by the maturational process associated with LC migration during steady-state conditions. Jian...

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Section: Subsets In Hiv-1 Transmissionmentioning

confidence: 99%

Section: Subsets In Hiv-1 Transmissionmentioning

confidence: 99%

Section: Subsets In Hiv-1 Transmissionmentioning

confidence: 99%

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Langerhans cells and viral immunity

2008

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“…The incomplete inhibition we observed using an anti-DC-SIGN mAb suggests the possible involvement of additional Env receptors, e.g. mannose receptor [7], and/or syndecan-3 [30]. The possibility that the marked virion endocytosis we observed in DC relies on the formation of HIV-1 Env-dependent virological synapselike structures [31,32], or whether it is simply the consequence of receptor-mediated cell-to-cell contiguity remains to be established.…”

Section: Discussionmentioning

confidence: 84%

DC contact with HIV‐1‐infected cells leads to high levels of Env‐mediated virion endocytosis coupled with enhanced HIV‐1 Ag presentation

et al. 2009

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In HIV-infected patients, DC are likely to interact with both cell-free HIV and HIV-infected cells. We were interested in investigating the mechanism of virus transmission occurring upon contact between HIV-1-infected cells and DC, as well as the consequences for HIV-1 Ag-presenting activity. By comparing mixed co-cultures with trans-well cultures, we observed that cell-to-cell contact strongly increased HIV-1 Env-mediated virion endocytosis in target DC. This endocytosis was independent of HIV-1 tropism, de novo infection, HIV-1 Env-CD4-dependent fusion, and immature DC activation/maturation. We also found that augmentation of HIV-1 endocytosis was closely correlated with strong, Env-dependent HIV-1 Ag presentation by DC. Our results provide a better understanding of the mechanisms underlying the induction of the anti-HIV adaptive immune response. © 2009 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim

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“…Various harmful substances can be produced by activated macrophages or microglia, which go on to damage other cells in the central nervous system (CNS) or induce apoptosis (Fu et al, 2014). Envelope glycoprotein gp120 (or gp120) is a glycoprotein found on the surface of the HIV envelope, and is essential for the virus' entry into cells as it plays a vital role in their attachment to specific cell-surface receptors (de Witte et al, 2007). Nuclear factor kappaB (NF-kappaB or NF-κB) proteins comprise a family of structurally related eukaryotic transcription factors that are involved in the control of a large number of normal cellular and organismal processes.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of naringin against gp120-induced injury mediated by P2X7 receptors in BV2 microglial cells

Chen

Qin

et al. 2016

Genet. Mol. Res.

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ABSTRACT. This study was aimed at exploring the effects of P2X 7 receptors on gp120-induced injury and naringin's protective effects against gp120-induced injury in BV2 microglia. BV2 microglia injury model was established by gp120 treatment and MTS assay was used to verify whether naringin has a cell-protective effect against gp120-induced injury. Changes in P2X 7 receptor expression were assayed using RT-PCR, qPCR, and western blot. Results showed that the ODs of the Ctrl, gp120, gp120+naringin, and gp120+BBG groups were 0.91 ± 0.10, 0.71 ± 0.09, 0.83 ± 0.10, and 0.83 ± 0.10, respectively. Compared to the control group, the gp120 group showed a significantly decreased cell survival rate. Cell survival rates of the gp120+naringin group increased significantly compared to those of the gp120 group, while no difference was observed when compared to the gp120+BBG group. The relative P2X 7 mRNA expression levels in the Ctrl, gp120, gp120+naringin, and gp120+BBG groups were 0.73 ± 0.06, 1.05 ± 0.06, 0.78 ± 0.05, and 0.81 ± 0.04, respectively. The corresponding P2X 7 protein expression levels were 0.46 ± 0.04, 0.79 ± 0.04, 0.38 ± 0.07, and 0.42 ± 0.06. P2X 7 mRNA and protein expression in the gp120 group increased significantly compared to those in the control group, and declined in the gp120+naringin group compared to those in the gp120 group. Therefore, P2X 7 receptors might be involved in gp120-induced injury in BV2 microglia, and naringin might play a protective role by inhibiting the up-regulated expression of P2X 7 receptors.

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Syndecan-3 is a dendritic cell-specific attachment receptor for HIV-1

Cited by 139 publications

References 49 publications

Langerhans cells and viral immunity

Langerhans cells and viral immunity

DC contact with HIV‐1‐infected cells leads to high levels of Env‐mediated virion endocytosis coupled with enhanced HIV‐1 Ag presentation

Protective effects of naringin against gp120-induced injury mediated by P2X7 receptors in BV2 microglial cells

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