Journal
JOURNAL OF NEUROVIROLOGY
Volume 8, Issue 6, Pages 585-598Publisher
SPRINGER
DOI: 10.1080/13550280290100950
Keywords
chemokine receptors; chemokines; fractalkine; HIV-1-associated dementia
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Funding
- NCRR NIH HHS [P20 RR15635-01] Funding Source: Medline
- NINDS NIH HHS [R01 NS41858-01] Funding Source: Medline
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Leukocyte migration and activation play an important role in immune surveillance and the pathogenesis of a variety of neurodegenerative disorders, including human immunodeficiency virus (HIV)-1-associated dementia (HAD). A novel chemokine named fractalkine (FKN, CX3CL1), which exists in both membrane-anchored and soluble isoforms, has been proposed to participate in the generation and progression of inflammatory brain disorders. Upon binding to the CX3C receptor one (CX3CR1), FKN induces adhesion, chemoattraction, and activation of leukocytes, including brain macrophages and microglia (MP). Constitutively expressed in the central nervous system (CNS), mainly by neurons, FKN is up-regulated and released in response to proinflammatory stimuli. Importantly, FKN is up-regulated in the brain tissue and cerebrospinal fluid (CSF) of HAD patients. Together, these observations suggest that FKN and its receptor have a unique role in regulating the neuroinflammatory events underlying disease. This review will examine how FKN contributes to the recruitment and activation of CX3CR1-expressing MP, which are critical events in the neuropathogenesis of HAD.
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