Role of Trophic Factors on Neuroimmunity in Neurodegenerative Infectious Diseases

Langford, Dianne; Masliah, Eliezer

doi:10.1080/13550280290100996

Cited by 16 publications

(13 citation statements)

References 125 publications

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“…HIV-1 Tat protein has been proposed as a key neuropathogenic factor in HIV-1-associated neurological diseases. Possible molecular pathways involve modulation of host gene expression by Tat protein internalized or expressed, intracellular signaling elicited by Tat binding to cell surface receptors, or both (10). Supporting these hypotheses is the evidence that HIV-1 Tat is secreted from Tat-expressing cells (11)(12)(13)(14) and HIV-infected cells (15,16) and is capable of interacting with molecules on the cell surface and entering cells in a biologically active form (17)(18)(19).…”

mentioning

confidence: 62%

Induction of C Chemokine XCL1 (Lymphotactin/Single C Motif-1α/Activation-Induced, T Cell-Derived and Chemokine-Related Cytokine) Expression by HIV-1 Tat Protein

Kim

Liu

Zhou

et al. 2004

The Journal of Immunology

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HIV-1 Tat has been proposed as a key agent in many AIDS-related disorders, including HIV-1-associated neurological diseases. We have recently shown that Tat expression induces a significant increase in T lymphocytes in the brains of Tat transgenic mice. The CNS infiltration of T lymphocytes has been noted in AIDS patients. In the present study using this unique genetic system we attempted to understand the underlying mechanisms of Tat expression-induced infiltration of T lymphocytes by examining chemokine expression. RNase protection assay revealed that in addition to CCL2 (monocyte chemoattractant protein-1), CCL3 (macrophage inflammatory protein-1α (MIP-1α)), CCL4 (MIP-1β), CCL5 (RANTES), CXCL2 (MIP-2), and CXCL10 (inducing protein-10), XCL1 (lymphotactin/single C motif-1α/activation-induced, T cell-derived and chemokine-related cytokine) was identified to be up-regulated by Tat expression. XCL1 is a C chemokine and plays a specific and important role in tissue-specific recruitment of T lymphocytes. Thus, we further determined the relationship between Tat and XCL1 expression. Tat-induced XCL1 expression was further confirmed by XCL1-specific RT-PCR and ELISA. Combined in situ hybridization and immunohistochemical staining identified astrocytes, monocytes, and macrophages/microglia as XCL1-producing cells in vivo. Using human astrocytes, U87.MG cells, as an in vitro model, activation of XCL1 expression was positively correlated with Tat expression. Moreover, the XCL1 promoter-driven reporter gene assay showed that Tat-induced XCL1 expression occurred at the transcriptional level. Taken together, these results demonstrate that Tat directly trans-activated XCL1 expression and suggest potential roles of Tat-induced XCL1 expression in the CNS infiltration of T lymphocytes during HIV-1 infection and subsequent HIV-1-induced neurological diseases.

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mentioning

confidence: 62%

Induction of C Chemokine XCL1 (Lymphotactin/Single C Motif-1α/Activation-Induced, T Cell-Derived and Chemokine-Related Cytokine) Expression by HIV-1 Tat Protein

Kim

Liu

Zhou

et al. 2004

The Journal of Immunology

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“…One is that the follow-up period of 1 year was insufficient, especially in the absence of control data on subjects not exposed to mine dust. Another limitation concerns the lack of data of co-affective factors such as serum leptin related with TNF-α [41,42] and neurotrophic factor related with IL-8 [43]. Serum cytokines can be measured by various techniques that include enzyme-linked immunosorbent assay (ELISA), cytokine flow cytometry, and biochip array [44].…”

Section: Discussionmentioning

confidence: 99%

Serum Levels of Interleukin-8 and Tumor Necrosis Factor-alpha in Coal Workers' Pneumoconiosis: One-year Follow-up Study

Lee¹,

Shin²,

Lee³

et al. 2010

Safety and Health at Work

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ObjectivesVarious cytokines induced by inhalation of coal dust may mediate inflammation and lead to tissue damage or fibrosis, such as coal workers' pneumoconiosis (CWP).MethodsTo investigate the relevance of serum cytokines in CWP, the levels of serum interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) as CWP biomarkers in 110 retired coal miners (22 controls and 88 CWP subjects) were related to cross sectional findings and 1-year progressive changes of the pneumoconiosis. Progressive changes of CWP were evaluated by paired comparison of chest radiographs. Analysis by a receiver operating characteristic curve assessed the biomarker potential of each cytokine.ResultsThe mean serum IL-8 level was significantly higher in CWP compared to controls and IL-8 levels correlated with the degree of CWP. The median serum TNF-α level was significantly higher in subjects with progressive CWP compared to subjects without CWP progression. The area under the ROC curve for IL-8 (0.70) and TNF-α (0.72) for CWP identification and progression, respectively, indicated the biomarker potential of the two cytokines. Serum cutoff values of IL-8 and TNF-α were 11.63 pg/mL (sensitivity, 69%; specificity, 64%) and 4.52 pg/mL (sensitivity, 67%; specificity, 79%), respectively.ConclusionThe results suggest that high levels of serum IL-8 are associated with the presence of CWP and those of serum TNF-α are associated with the progression of CWP.

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“…Viral proteins such as Tat and gp120 can dysregulate growth factor signaling cascades in a number of ways. For example, through molecular mimicry, viral proteins can exploit the host cell’s machinery by binding to receptors and disrupting normal host cell signaling [79,80]. For instance, molecular mimicry between gp41 and the astrocytic protein α-actinin, originally revealed by antibody cross-reactivity, allows gp41 to bind to astrocyte cell membranes and induce aberrant signaling [81].…”

Section: Hiv and Neurotrophic Signalingmentioning

confidence: 99%

Neuronal Toxicity in HIV CNS Disease

Kovalevich

Langford

2012

Future Virol.

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HIV enters the brain during the early stages of initial infection and can result in a complicated array of diverse neurological dysfunctions. While neuronal injury and loss are at the heart of neurological decline and HIV-associated neuropathology, HIV does not productively infect neurons and the effects of HIV on neurons may be described as largely indirect. Viral proteins released from infected cells in the CNS are a well-characterized source of neuronal toxicity. Likewise, host-derived inflammatory cytokines and chemokines released from infected and/or activated glial cells can damage neurons, as well. Newly identified host–virus interactions and the current state of our knowledge regarding HIV-associated neuronal toxicity will be addressed in this review. Aspects of HIV-associated neurotoxic mechanisms, patterns of neuronal damage, viral effects on neurotrophic signaling, clade variations and comorbid substance abuse will be discussed. Recent advances in our understanding of the impact of HIV infection of the CNS on neuronal dysfunction and cell death will also be highlighted.

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Role of Trophic Factors on Neuroimmunity in Neurodegenerative Infectious Diseases

Cited by 16 publications

References 125 publications

Induction of C Chemokine XCL1 (Lymphotactin/Single C Motif-1α/Activation-Induced, T Cell-Derived and Chemokine-Related Cytokine) Expression by HIV-1 Tat Protein

Induction of C Chemokine XCL1 (Lymphotactin/Single C Motif-1α/Activation-Induced, T Cell-Derived and Chemokine-Related Cytokine) Expression by HIV-1 Tat Protein

Serum Levels of Interleukin-8 and Tumor Necrosis Factor-alpha in Coal Workers' Pneumoconiosis: One-year Follow-up Study

Neuronal Toxicity in HIV CNS Disease

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