Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 81, Issue 6, Pages 1504-1511Publisher
WILEY
DOI: 10.1189/jlb.1106711
Keywords
HIV; AIDS; macrophage
Categories
Funding
- NIMH NIH HHS [MH62261, P30 MH062261-06A1, R01 MH073490-02, MH073490, P30 MH062261, R01 MH073490] Funding Source: Medline
- NINDS NIH HHS [R01 NS045534-04, NS045534, F32 NS048830, R01 NS045534] Funding Source: Medline
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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.
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