DC-SIGN and CLEC-2 Mediate Human Immunodeficiency Virus Type 1 Capture by Platelets

Chaipan, Chawaree; Soilleux, Elizabeth; Simpson, Peter; Hofmann, Heike; Gramberg, Thomas; Marzi, Andrea; Geier, Martina; Stewart, Elizabeth A.; Eisemann, Jutta; Steinkasserer, Alexander; Suzuki‐Inoue, Katsue; Fuller, Gemma L.J.; Pearce, Andrew C.; Watson, Steve P.; Hoxie, James A.; Baribaud, Frédéric; Pöhlmann, Stefan

doi:10.1128/jvi.00136-06

Cited by 232 publications

(231 citation statements)

References 66 publications

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“…Thus, CXCL4 may play a dual role in the pathogenesis of HIV-1 disease, on one side by suppressing HIV-1 replication but on the other by fostering immunologic activation, inflammation, and coagulation abnormalities. In this context, binding of HIV-1 virions to CXCL4 deposited on the surface of platelets could act as a trigger for further platelet activation and CXCL4 release, in a similar fashion to the putative effects of HIV-1 binding to CLEC-2 and DC-SIGN on the platelet membrane (23).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, platelet alterations, including abnormal platelet activation and apoptosis, are frequently detected in HIV-1-infected individuals even with normal platelet counts (21,22). Sustained platelet activation in these subjects may be due, at least in part, to direct binding and internalization of HIV-1 virions by platelets, mediated by the C-type lectin receptors CLEC-2 and DC-SIGN (23).…”

mentioning

confidence: 99%

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Identification of the platelet-derived chemokine CXCL4/PF-4 as a broad-spectrum HIV-1 inhibitor

Auerbach

Yin

Miao

et al. 2012

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

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The natural history of HIV-1 infection is highly variable in different individuals, spanning from a rapidly progressive course to a longterm asymptomatic infection. A major determinant of the pace of disease progression is the in vivo level of HIV-1 replication, which is regulated by a complex network of cytokines and chemokines expressed by immune and inflammatory cells. The chemokine system is critically involved in the control of HIV-1 replication by virtue of the role played by specific chemokine receptors, most notably CCR5 and CXCR4, as cell-surface coreceptors for HIV-1 entry; hence, the chemokines that naturally bind such coreceptors act as endogenous inhibitors of HIV-1. Here, we show that the CXC chemokine CXCL4 (PF-4), the most abundant protein contained within the α-granules of platelets, is a broad-spectrum inhibitor of HIV-1 infection. Unlike other known HIV-suppressive chemokines, CXCL4 inhibits infection by the majority of primary HIV-1 isolates regardless of their coreceptor-usage phenotype or genetic subtype. Consistent with the lack of viral phenotype specificity, blockade of HIV- 1 infection occurs at the level of virus attachment and entry via a unique mechanism that involves direct interaction of CXCL4 with the major viral envelope glycoprotein, gp120. The binding site for CXCL4 was mapped to a region of the gp120 outer domain proximal to the CD4-binding site. The identification of a platelet-derived chemokine as an endogenous antiviral factor may have relevance for the pathogenesis and treatment of HIV-1 infection

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Identification of the platelet-derived chemokine CXCL4/PF-4 as a broad-spectrum HIV-1 inhibitor

Auerbach

Yin

Miao

et al. 2012

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

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“…Some insight into this function might be gained from other CLR expressed by hepatocytes, LSEC, and KC. LSEC and KC express various CLR, including CLEC2 (34,35) and CD209 (36,37), which facilitate their scavenging activities and their ability to process Ags for T cell interactions (38). The asialoglycoprotein receptor is a CLR abundantly expressed on hepatocytes (6).…”

Section: Cd169mentioning

confidence: 99%

Characterization of the Expression and Function of the C-Type Lectin Receptor CD302 in Mice and Humans Reveals a Role in Dendritic Cell Migration

Silveira

Fromm

et al. 2016

The Journal of Immunology

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C-type lectin receptors play important roles in immune cell interactions with the environment. We described CD302 as the simplest, single domain, type I C-type lectin receptor and showed it was expressed mainly on the myeloid phagocytes in human blood. CD302 colocalized with podosomes and lamellopodia structures, so we hypothesized that it played a role in cell adhesion or migration. In this study, we used mouse models to obtain further insights into CD302 expression and its potential immunological function. Mouse CD302 transcripts were, as in humans, highest in the liver, followed by lungs, lymph nodes (LN), spleen, and bone marrow. In liver, CD302 was expressed by hepatocytes, liver sinusoidal endothelial cells, and Kupffer cells. A detailed analysis of CD302 transcription in mouse immune cells revealed highest expression by myeloid cells, particularly macrophages, granulocytes, and myeloid dendritic cells (mDC). Interestingly, 2.5-fold more CD302 was found in migratory compared with resident mDC populations and higher CD302 expression in mouse M1 versus M2 macrophages was also noteworthy. CD302 knockout (CD302KO) mice were generated. Studies on the relevant immune cell populations revealed a decrease in the frequency and numbers of migratory mDC within CD302KO LN compared with wild-type LN. In vitro studies showed CD302KO and wild-type DC had an equivalent capacity to undergo maturation, prime T cells, uptake Ags, and migrate toward the CCL19/CCL21 chemokines. Nevertheless, CD302KO migratory DC exhibited reduced in vivo migration into LN, confirming a functional role for CD302 in mDC migration.

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“…It is notable that platelets contain two C-type lectins, C-type lectin-like receptor 2 (CLEC-2) and dendritic cell-specific, ICAM-3 grabbing, nonintegrin (DC-SIGN), that are each surfaceexpressed proteins that exhibit calcium-dependent binding of infectious HIV-1 particles (Boukour et al, 2006;Chaipan et al, 2006;Flaujac et al, 2010). Although it has been suggested that platelets might represent a circulating reservoir for HIV-1, it has also been reported that internalization of HIV-1 by platelets might cause disrupt viral integrity (Boukour et al, 2006;Flaujac et al, 2010).…”

Section: Contaminating Cell Types As Potential Targets For Binding Ofmentioning

confidence: 99%

Interactions of Infectious HIV-1 Virions with Erythrocytes: Implications for HIV-1 Pathogenesis and Infectivity

Beck¹,

Alving²

2011

HIV-Host Interactions

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DC-SIGN and CLEC-2 Mediate Human Immunodeficiency Virus Type 1 Capture by Platelets

Cited by 232 publications

References 66 publications

Identification of the platelet-derived chemokine CXCL4/PF-4 as a broad-spectrum HIV-1 inhibitor

Identification of the platelet-derived chemokine CXCL4/PF-4 as a broad-spectrum HIV-1 inhibitor

Characterization of the Expression and Function of the C-Type Lectin Receptor CD302 in Mice and Humans Reveals a Role in Dendritic Cell Migration

Interactions of Infectious HIV-1 Virions with Erythrocytes: Implications for HIV-1 Pathogenesis and Infectivity

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