Dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin mediates HIV-1 infection of and transmission by M2a-polarized macrophages in vitro

Cassol, Edana; Cassetta, Luca; Rizzi, Chiara; Gabuzda, Dana; Alfano, Massimo; Poli, Guido

doi:10.1097/qad.0b013e32835cfc82

Cited by 21 publications

(16 citation statements)

References 41 publications

(72 reference statements)

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“…IL-13 also promotes differentiation of B cells into Ab-secreting plasma cells. M2 macrophages express more DC-SIGN than M1 macrophages (Cassol et al, 2012), supporting the concept that M2 macrophages are likely to serve as a more efficient target cell for HHV-8 infection. Importantly, multiple receptors are needed for efficient infection of these macrophages by HHV-8.…”

Section: Hhv-8 Infection Of Professional Apcmentioning

confidence: 76%

Professional antigen presenting cells in human herpesvirus 8 infection

Knowlton¹,

Lepone²,

Li³

et al. 2013

Front. Immun.

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Professional antigen presenting cells (APC), i.e., dendritic cells (DC), monocytes/macrophages, and B lymphocytes, are critically important in the recognition of an invading pathogen and presentation of antigens to the T cell-mediated arm of immunity. Human herpesvirus 8 (HHV-8) is one of the few human viruses that primarily targets these APC for infection, altering their cytokine profiles, manipulating their surface expression of MHC molecules, and altering their ability to activate HHV-8-specific T cells. This could be why T cell responses to HHV-8 antigens are not very robust. Of these APC, only B cells support complete, lytic HHV-8 infection. However, both complete and abortive virus replication cycles in APC could directly affect viral pathogenesis and progression to Kaposi's sarcoma (KS) and HHV-8-associated B cell cancers. In this review, we discuss the effects of HHV-8 infection on professional APC and their relationship to the development of KS and B cell lymphomas.

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Section: Hhv-8 Infection Of Professional Apcmentioning

confidence: 76%

Professional antigen presenting cells in human herpesvirus 8 infection

Knowlton¹,

Lepone²,

Li³

et al. 2013

Front. Immun.

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“…In the nodes, mDC activate the specific CD4 + T cells that become infected by a “kiss of death” delivered by the DC-SIGN associated virus. DC-SIGN expression has been later described in other cells such as macrophages 8, 9 where it likely plays a similar role 9. Other molecules, such as CD206/mannose receptor have been also credited with similar functions in the context of HIV infection 10.…”

Section: Hiv Entry Into Cd4+ Cells Of the Immune Systemmentioning

confidence: 99%

The Puzzling Role of CXCR4 in Human Immunodeficiency Virus Infection

Vicenzi¹,

Lió²,

Poli³

2013

Theranostics

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The human immunodeficiency virus type-1 (HIV-1) is the etiological agent of the acquired immunodeficiency syndrome (AIDS), a disease highly lethal in the absence of combination antiretroviral therapy. HIV infects CD4+ cells of the immune system (T cells, monocyte-macrophages and dendritic cells) via interaction with a universal primary receptor, the CD4 molecule, followed by a mandatory interaction with a second receptor (co-receptor) belonging to the chemokine receptor family. Apart from some rare cases, two chemokine receptors have been evolutionarily selected to accomplish this need for HIV-1: CCR5 and CXCR4. Yet, usage of these two receptors appears to be neither casual nor simply explained by their levels of cell surface expression. While CCR5 use is the universal rule at the start of every infection regardless of the transmission route (blood-related, sexual or mother to child), CXCR4 utilization emerges later in disease coinciding with the immunological deficient phase of infection. Moreover, in most instances CXCR4 use as viral entry co-receptor is associated with maintenance of CCR5 use. Since antiviral agents preventing CCR5 utilization by the virus are already in use, while others targeting either CCR5 or CXCR4 (or both) are under investigation, understanding the biological correlates of this “asymmetrical” utilization of HIV entry co-receptors bears relevance for the clinical choice of which therapeutics should be administered to infected individuals. We will here summarize the basic knowledge and the hypotheses underlying the puzzling and yet unequivocal role of CXCR4 in HIV-1 infection.

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“…14,15,40 Recently, we have reported that expression of dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin is present and enhanced in unpolarized and M2a-MDM, respectively, whereas it downregulates M1-cells, 21 therefore representing a potentially useful marker to distinguish between M1-and M2-macrophages in vivo. Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin expression by M2a-MDM, on the one hand, may compensate for the decreased levels of CD4 on the surface of these cells, but, on the other hand, facilitate virion transmission to CD4 + T cells, in analogy to its already demonstrated role in dendritic cell.…”

Section: Macrophage Polarization and Hiv-1 Infectionmentioning

confidence: 99%