Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 81, Issue 3, Pages 436-446Publisher
WILEY
DOI: 10.1002/jnr.20486
Keywords
chemokines; Alzheimer's disease; multiple sclerosis; migration; neurotoxicity
Categories
Funding
- NIAID NIH HHS [AI-051519] Funding Source: Medline
- NIMH NIH HHS [K01 MH076679, MH070297, MH52974] Funding Source: Medline
- NINDS NIH HHS [NS11920, T32NS07098] Funding Source: Medline
Ask authors/readers for more resources
Microglia are the resident phagocytes of the brain and are an important source of proinflammatory mediators. Human immunodeficiency virus (HIV)-1 infects the central nervous system early in the course of disease, and it is believed that this occurs, in part, through the transmigration of HIV-1-infected cells across the blood-brain barrier. Infected cells release viral proteins, such as Tat and gp120. After microglia interact with these proteins, they become activated and secrete chemokines; upregulate key surface receptors, such as CD40, and also activate resident cells. This review focuses on the consequences of microglial activation in NeuroAIDS, with an emphasis on chemokine production and CD40 upregulation after interaction with tat or gp120. The importance of microglial CD40 in two other neurological diseases, Alzheimer's disease and multiple sclerosis, is also discussed. (c) 2005 Wiley-Liss, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available