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Originally published online as doi:10.1189/jlb.0306135 on August 15, 2006

Published online before print August 15, 2006
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(Journal of Leukocyte Biology. 2006;80:994-1000.)
© 2006 by Society for Leukocyte Biology

Role of gp120 in dendritic cell dysfunction in HIV infection

Claire Chougnet* and Sandra Gessani{dagger},1

* Division of Molecular Immunology, Cincinnati Children’s Hospital Research Foundation and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; and
{dagger} Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy

1 Correspondence: Istituto Superiore di Sanità, Department of Cell Biology and Neurosciences, Viale Regina Elena 299, Via Castro Laurenziano 10, Rome, Rome 00161, Italy. E-mail: sandra.gessani{at}iss.it

Only a limited fraction of circulating virions are demonstrably infectious; therefore, exposure to inactivated viruses may mimic the most frequent type of CD4-HIV interactions that occur in vivo. Several studies have recently underscored the crucial role that those noninfectious viruses could play in defective immune function in HIV-infected individuals and in particular, in the dysregulation of dendritic cell (DC) function. In this review, we discuss how interactions between DC and HIV gp120 or inactivated virus, which harbor intact surface gp120, lead to impaired DC function through direct (direct contact) or indirect mechanisms (as a consequence of primary CD4+ T cell dysregulation, followed by defective CD4-DC interactions). It is important that these functionally impaired DCs fail to give optimal signal to T cells but appear to favor the emergence of regulatory T cells. gp120-mediated impairment of DC function could therefore play an important role in the pathogenesis of HIV disease.

Key Words: T cells • AIDS pathogenesis • immune regulation




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