IL‐16 expression in lymphocytes and microglia in HIV‐1 encephalitis

Zhao, Meng; Si, Qiusheng; Lee, S. C.

doi:10.1046/j.0305-1846.2003.00527.x

Cited by 26 publications

(18 citation statements)

References 34 publications

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“…However, infiltrating lymphocytes and activated microglia in brains with HIV-1 encephalitis might show strong immunoreactivity for IL-16, a natural ligand of CD4. Because this cytokine inhibits HIV-1 propagation, lymphocytes might contribute to an innate antiviral immune response in the CNS in addition to microglia (Zhao et al, 2004). Furthermore, IL-4 and interferon (IFN)-g, two cytokines with important roles in immune regulation, are produced by different lymphocyte populations and seem to induce in microglia a cytoprotective phenotype (Butovsky et al, 2005).…”

Section: From Neuropathology Of Hiv Infection To Development Of Mcmd/hadmentioning

confidence: 98%

Mechanisms of Neuroimmunity and Neurodegeneration Associated with HIV-1 Infection and AIDS

Kaul

Lipton

2006

Jrnl NeuroImmune Pharm

102

101

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Infection with the human immunodeficiency virus-1 (HIV-1) and acquired immunodeficiency syndrome (AIDS) are a persistent health problem worldwide. HIV-1 seems to enter the brain very soon after peripheral infection and can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction, and frank dementia. Infected peripheral immune-competent cells, in particular macrophages, appear to infiltrate the CNS and provoke a neuropathological response involving all cell types in the brain. The course of HIV-1 disease is strongly influenced by viral and host factors, such as the viral strain and the response of the host's immune system. In addition, HIV-1-dependent disease processes in the periphery have a substantial effect on the pathological changes in the central nervous system (CNS), although the brain eventually harbors a distinctive viral population of its own. In the CNS, HIV-1 also incites activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes, and glutamate receptor-mediated excitotoxicity, all of which can initiate numerous downstream signaling pathways and disturb neuronal and glial function. Although there have been many major improvements in the control of viral infection in the periphery, an effective therapy for HIV-1-associated dementia (HAD) is still not available. This article addresses recently uncovered pathologic neuroimmune and degenerative mechanisms contributing to neuronal damage induced by HIV-1 and discusses experimental and potentially future therapeutic approaches.

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Section: From Neuropathology Of Hiv Infection To Development Of Mcmd/hadmentioning

confidence: 98%

Mechanisms of Neuroimmunity and Neurodegeneration Associated with HIV-1 Infection and AIDS

Kaul

Lipton

2006

Jrnl NeuroImmune Pharm

102

101

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show abstract

“…However, infiltrating lymphocytes and activated microglia in brains with HIV-1 encephalitis might show strong immunoreactivity for IL-16, a natural ligand of CD4 that inhibits HIV-1 propagation. Thus, lymphocytes might contribute to an innate antiviral immune response in the CNS in addition to microglia [137]. Furthermore, different lymphocyte populations produce IL-4 and interferon (IFN)-, two cytokines with important roles in immune regulation that seem to induce in microglia a cytoprotective phenotype [15].…”

Section: Neuropathology Of Hiv Infection and Development Of Hadmentioning

confidence: 99%

Mechanisms of Neuronal Injury and Death in HIV-1 Associated Dementia

Kaul

Lipton²

2006

CHR

153

107

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Infection with the human immunodeficiency virus-1 (HIV-1) and acquired immunodeficiency syndrome (AIDS) remain a persistent and even growing health problem worldwide. Besides its detrimental systemic effects on the immune system, HIV-1 seems to enter the brain very soon after peripheral infection and can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction and frank dementia. Infected peripheral immune cells, in particular macrophages, appear to infiltrate the CNS and provoke a neuropathological response involving all cell types in the brain. Both viral and host factors, such as the viral strain and the response of the host's immune system, strongly influence the course of HIV-1 disease. Moreover, HIV-1-dependent disease processes in the periphery have a substantial effect on the pathology developing in the central nervous system (CNS), although the brain eventually harbors a distinctive viral population of its own. In the CNS, HIV-1 also initiates activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes and glutamate receptor-mediated excitotoxicity, all of which can activate numerous downstream signaling pathways and disturb neuronal and glial function. Although there have been substantial improvements in the control of viral infection in the periphery, an effective therapy for HIV-1 associated dementia (HAD) is still not in sight. This article will review recently identified injurious mechanisms potentially contributing to neuronal death in association with HIV-1 disease and discuss recent and prospective approaches for therapy and prevention of HAD.

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“…Since this cytokine inhibits HIV-1 propagation, lymphocytes might contribute to an innate antiviral immune response in the CNS in addition to microglia. 37 Cell migration also engages adhesion molecules, and increased expression of vascular cell adhesion molecule-1 (VCAM-1) has been implicated in mononuclear cell migration into the brain during HIV and SIV infection. 30,31,38 As an alternative to entry via infected macrophages, it has been suggested that the inflammatory cytokine, tumor necrosis factor-alpha (TNF-a), promotes a paracellular route for HIV-1 across the BBB.…”

Section: From Hiv Entry Into the Brain To Development Of Mcmd/hadmentioning

confidence: 99%

“…Therapeutic concentrations of VPA (0.6 mM) resulted in (1) significant increases in both nuclear and cytoplasmic bcatenin protein levels; (2) decreases in the level of protein akinase C and epsilon isozymes 182 and (3) downregulation of myristoylated alanine-rich C-kinase substrate (MARCKS) 183 through inositol-independent mechanisms. 184 VPA-mediated neuroprotection involves diminished activity of GSK-3b via the inhibition of phosphorylation of b-catenin (Ser 33,37 ) and tau (Ser 202 and Thr 181 ), 185 as well as the overall increase in total b-catenin protein levels (Figure 3). Hyperphosphorylation of b-Catenin and tau directly affects neuronal apoptosis and dysfunction.…”

mentioning

confidence: 99%

HIV-1 infection and AIDS: consequences for the central nervous system

et al. 2005

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Infection with the human immunodeficiency virus-1 (HIV-1) can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction and frank dementia. After infiltrating peripheral immune competent cells, in particular macrophages, HIV-1 provokes a neuropathological response involving all cell types in the brain. HIV-1 also incites activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes and glutamate receptor-mediated excitotoxicity, all of which can trigger numerous downstream signaling pathways and disrupt neuronal and glial function. This review will discuss recently uncovered pathologic neuroimmune and degenerative mechanisms contributing to neuronal damage induced by HIV-1 and potential approaches for development of future therapeutic intervention.

show abstract

IL‐16 expression in lymphocytes and microglia in HIV‐1 encephalitis

Cited by 26 publications

References 34 publications

Mechanisms of Neuroimmunity and Neurodegeneration Associated with HIV-1 Infection and AIDS

Mechanisms of Neuroimmunity and Neurodegeneration Associated with HIV-1 Infection and AIDS

Mechanisms of Neuronal Injury and Death in HIV-1 Associated Dementia

HIV-1 infection and AIDS: consequences for the central nervous system

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