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Originally published online as doi:10.1189/jlb.1106711 on March 16, 2007

Published online before print March 16, 2007
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(Journal of Leukocyte Biology. 2007;81:1504-1511.)
© 2007 by Society for Leukocyte Biology

Osteopontin prevents monocyte recirculation and apoptosis

Tricia H. Burdo*, Malcolm R. Wood{dagger} and Howard S. Fox*,1

* Molecular and Integrative Neurosciences Department and
{dagger} Core Microscopy Facility, The Scripps Research Institute, La Jolla, California, USA

1 Correspondence: Molecular and Integrative Neuroscience Department, The Scripps Research Institute, 10550 North Torrey Pines Rd., SP30-2030, La Jolla, CA 92037, USA. E-mail: hsfox{at}scripps.edu

Cells of the monocyte/macrophage lineage have been shown to be the principal targets for productive HIV-1 replication within the CNS. In addition, HIV-1-associated dementia (HAD) has been shown to correlate with macrophage abundance in the brain. Although increased entry of monocytes into the brain is thought to initiate this process, mechanisms that prevent macrophage egress from the brain and means that prevent macrophage death may also contribute to cell accumulation. We hypothesized that osteopontin (OPN) was involved in the accumulation of macrophages in the brain in neuroAIDS. Using in vitro model systems, we have demonstrated the role of OPN in two distinct aspects of macrophage accumulation: prevention from recirculation and protection from apoptosis. In these unique mechanisms, OPN would aid in macrophage survival and accumulation in the brain, the pathological substrate of HAD.

Key Words: HIV • AIDS • macrophage




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