Intercellular adhesion molecules (ICAM)‐1 ICAM‐2 and ICAM‐3 function as counter‐receptors for lymphocyte function‐associated molecule 1 in human immunodeficiency virus‐mediated syncytia formation

Butini, Luca; Fougerolles, Antonin R. de; Vaccarezza, Mauro; Graziosi, Cecilia; Cohen, David I.; Montroni, M; Springer, Timothy A.; Pantaleo, Giuseppe; Fauci, Anthony S.

doi:10.1002/eji.1830240939

Cited by 46 publications

(29 citation statements)

References 40 publications

(2 reference statements)

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“…Hildreth and Orentas (11) were the first to show that antibodies to LFA-1 inhibited syncytium formation induced by HIV. This finding was corroborated by other investigators who showed that syncytium formation in HIV-infected cultures was blocked by antibodies to the three ICAM ligands (2). The LFA-1/ ICAM-1 interaction was also found to be important for conjugation between HIV-infected dendritic cells and CD4 ϩ T cells in the absence of any syncytium formation (20).…”

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confidence: 80%

LFA-1 Expression on Target Cells Promotes Human Immunodeficiency Virus Type 1 Infection and Transmission

Hioe

Chien

et al. 2001

J Virol

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While the interaction of the human immunodeficiency virus (HIV) envelope glycoprotein gp120 with CD4 and the chemokine receptors CXCR4 and CCR5 is clearly required to initiate HIV infection, it has now become evident that other cell membrane proteins, including the major adhesion molecule LFA-1 (CD11a/CD18) and its ligands ICAM-1, ICAM-2, and ICAM-3, are also involved in HIV infection (reviewed in reference 12). These molecules are expressed on cells that serve as hosts for the virus, as well as on the envelopes of HIV virions. Previous studies by Fortin et al. (6) and Rizutto and Sodroski (18) demonstrated that ICAM-1 incorporated into the envelopes of HIV virions increased the infectivity of the virus 2-to 10-fold. These results suggest that ICAM-1 molecules present on the surfaces of HIV virions are functional and capable of interacting with the LFA-1 receptor on the target cell surface and that this interaction facilitates virus binding to and entry into the cell.LFA-1 and its ICAM ligands have also been shown to be necessary for syncytium formation in HIV-infected cultures and for efficient cell-to-cell transmission of the virus. Hildreth and Orentas (11) were the first to show that antibodies to LFA-1 inhibited syncytium formation induced by HIV. This finding was corroborated by other investigators who showed that syncytium formation in HIV-infected cultures was blocked by antibodies to the three ICAM ligands (2). The LFA-1/ ICAM-1 interaction was also found to be important for conjugation between HIV-infected dendritic cells and CD4 ϩ T cells in the absence of any syncytium formation (20). Blocking such interactions by monoclonal antibodies (MAbs) to LFA-1 or ICAM-1 reduced virus transfer from the dendritic cells to the T cells. Most recently, a dendritic-cell-specific C-type lectin, DC-SIGN, which binds ICAM-3 with high affinity, has been shown to play a role in promoting the capture of HIV type 1 (HIV-1) by dendritic cells and facilitating the transmission of the virus to CD4 ϩ T cells (8, 9). LFA-1 is also known to affect HIV neutralization by virusspecific antibodies. Gomez and Hildreth (10) and Hioe et al. (13) demonstrated that HIV neutralization by HIV-positive plasma or by anti-gp120 MAbs was enhanced in the presence of MAbs to LFA-1. Hioe et al. (13) further showed that enhanced neutralization was observed when the anti-LFA-1 MAbs were present only during the initial 24 h of virus infection or were added 24 h postinfection. These results suggest that the anti-LFA-1 MAbs could act on different stages of HIV-1 infection, including the initial virus-cell interaction as well as the replication and spread of the virus from cell to cell.Although previous studies have indicated that LFA-1 and its ICAM ligands are involved in multiple stages of HIV infection, little work has been done to determine to what extent the expression and activation state of LFA-1 on cells targeted by HIV affect virus infection and transmission. HIV-1 virions bearing ICAM-1 were more infectious than their ICAM-1-negative co...

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confidence: 80%

LFA-1 Expression on Target Cells Promotes Human Immunodeficiency Virus Type 1 Infection and Transmission

Hioe

Chien

et al. 2001

J Virol

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“…However, the complete inhibition of THP-1 cell adhesion by anti-ICAM-1 antibody was not achieved, suggesting other molecules, such as ICAM-2 and ICAM-3, may be involved in this adhesion event induced by gp120. There is evidence that ICAM-2 and ICAM-3, in addition to ICAM-1, can function as ligands in HIVmediated syncytia formation (Butini et al, 1994). Thus, it will be important to determine whether gp120 affects the expression of ICAM-2 and/or ICAM-3 in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

Ren

Yao

Chen

2002

Laboratory Investigation

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SUMMARY:Human immunodeficiency virus type 1 (HIV-1) infection is often associated with central nervous system damage and vascular complications. However, the mechanisms of this association are largely unknown. We examined the effect of HIV-1 envelope glycoprotein 120 (gp120) on cell adhesion molecule expression by endothelial cells. We found, for the first time, that both soluble and membrane-bound gp120 could significantly increase the expression of human endothelial intercellular adhesion molecule-1 (ICAM-1) at both mRNA and protein levels, but not vascular cell adhesion molecule-1 and E-selectin. The specificity of gp120-mediated response was demonstrated by blocking experiments using a specific monoclonal antibody against gp120, which successfully abolished the gp120-mediated increase of ICAM-1 expression. Furthermore, there was a significant increase of human monocytic cell line THP-1 adherence onto the gp120-treated endothelial monolayers. This increased cell adhesion was effectively blocked by either anti-gp120 or anti-ICAM antibodies. These findings suggest that HIV-1 gp120-mediated endothelial ICAM-1 expression could be one of the important mechanisms of HIV-1 pathogenesis. (Lab Invest 2002, 82:245-255). B oth human immunodeficiency virus (HIV)-positiveand acquired immune deficiency syndrome (AIDS) patients often have significantly increased levels of circulating cell adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) (Greenwood et al, 1998; Seigneur et al, 1997). Serum ICAM-1 levels correlate well with AIDS progression in HIV type 1 (HIV-1)-infected patients (Galea et al, 1997). Endothelial cells and leukocytes from these patients exhibit a significant increase of such adhesion molecules (Pillet et al, 1999;Zietz et al, 1996). HIV-1 particles also incorporate many cell adhesion molecules (Guo and Hildreth, 1995). HIV-associated ICAM-1 is biologically active and can enhance virus infectivity (Fortin et al, 1997) and virus-induced syncytium formation (Gruber et al, 1991). ICAM-1-bearing viruses are less susceptible to neutralization by anti-envelope glycoprotein 120 (gp120) monoclonal antibodies than the same virus produced in cells expressing no ICAM-1 (Sawyer et al, 1994). HIV-1 replication in monocytes/macrophages is significantly enhanced by interaction with endothelial cells through cell adhesion molecules (Gilles et al, 1995). In addition, alterations in expression of cell adhesion molecules by leukocytes and endothelial cells can increase leukocyte migration into the tissues, which may result in certain organ damage. Indeed, HIV-1-infected leukocytes can transmigrate into the central nervous system and cause encephalopathy (Nottet, 1999). Endothelial cell dysfunction and leukocyte infiltration may also be attributable to the increased frequency of vascular complications such as atherosclerosis in HIV-1-infected patients (Constans et al, 1995;Tabib et al, 2000).Several factors may contribute to the increased levels of cell adhesion mole...

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“…In parallel, aliquots of 10 5 cocultured and unmixed PMNLs were tested by different assays for the total amount of viral nucleic acids. Then, the copy number of viral DNA, IE mRNA, and pp67 mRNA per infected PMNL was calculated by dividing the total copy number for each viral nucleic acid per 10 5 PMNLs by the number of PMNLs positive for each parameter. In addition, the number of p72-and pp65-positive PMNLs and the number of PMNLs carrying infectious virus was determined according to well-standardized procedures (see below).…”

Section: Cell Cultures and Virus Strainsmentioning

confidence: 99%

Human Cytomegalovirus Replicates Abortively in Polymorphonuclear Leukocytes after Transfer from Infected Endothelial Cells via Transient Microfusion Events

Gerna¹,

Percivalle²,

Baldanti³

et al. 2000

J Virol

148

168

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Intercellular adhesion molecules (ICAM)‐1 ICAM‐2 and ICAM‐3 function as counter‐receptors for lymphocyte function‐associated molecule 1 in human immunodeficiency virus‐mediated syncytia formation

Cited by 46 publications

References 40 publications

LFA-1 Expression on Target Cells Promotes Human Immunodeficiency Virus Type 1 Infection and Transmission

LFA-1 Expression on Target Cells Promotes Human Immunodeficiency Virus Type 1 Infection and Transmission

HIV-1 Envelope Glycoprotein 120 Increases Intercellular Adhesion Molecule-1 Expression by Human Endothelial Cells

Human Cytomegalovirus Replicates Abortively in Polymorphonuclear Leukocytes after Transfer from Infected Endothelial Cells via Transient Microfusion Events

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