Interferon-Independent, Human Immunodeficiency Virus Type 1 gp120-Mediated Induction of CXCL10/IP-10 Gene Expression by Astrocytes In Vivo and In Vitro

Asensio, Valérie C.; Maier, Joachim; Milner, Richard; Boztuğ, Kaan; Kincaid, Carrie; Moulard, Maxime; Phillipson, Curtis; Lindsley, Kristen; Krucker, Thomas; Fox, Howard S.; Campbell, Iain L.

doi:10.1128/jvi.75.15.7067-7077.2001

Cited by 122 publications

(110 citation statements)

References 68 publications

Supporting

Mentioning

102

Contrasting

Unclassified

Order By: Relevance

“…The astrocytosis was further investigated by quantitative reverse transcriptase-PCR expression analysis of the CXC chemokines CXCL9 and CXCL10, which are in the central nervous system predominantly produced by reactive astrocytes. 34,35 CXCL9 and CXCL10 mRNA levels were found to be 4.2 and 7.4 times higher at 125 dpi in the wild-type control brains compared to the IL-1RI Ϫ/Ϫ mice, respectively. At the terminal stage of the disease the expression of CXCL9 and CXCL10 was 8.3-and 4.6-fold increased in the scrapie-infected C57/B6 controls ( Figure 3).…”

Section: Resultsmentioning

confidence: 94%

Role of Interleukin-1 in Prion Disease-Associated Astrocyte Activation

Schultz

Schwarz

Neidhold

et al. 2004

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 94%

Role of Interleukin-1 in Prion Disease-Associated Astrocyte Activation

Schultz

Schwarz

Neidhold

et al. 2004

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…3A). A number of investigators have reported the induction of chemokines, including CXCL10, in a variety of cell types by gp120 (14,15,22). We addressed the requirement for viral gp120 in the induction of CXCL10 and CXCL11 in MDM using pseudotyped virus lacking gp120/41, but containing the VSV-G envelope protein.…”

Section: Resultsmentioning

confidence: 99%

“…Some investigators have reported induction of chemokines in monocyte/macrophages (14,15) and astrocytes (22) by gp120 or extracellular Tat (23). As noted above, the induction we found for CXCL10 and CXCL11 required viral infection, could occur with pseudotyped virus lacking gp120/41, and was not due to secreted factors.…”

Section: Figurementioning

confidence: 99%

Roles for CXC Chemokine Ligands 10 and 11 in Recruiting CD4+ T Cells to HIV-1-Infected Monocyte-Derived Macrophages, Dendritic Cells, and Lymph Nodes

Foley

Solow

et al. 2005

The Journal of Immunology

View full text Add to dashboard Cite

We investigated roles for chemoattractants in dissemination of HIV-1 by examining the induction of T cell-active chemokines in HIV-1-infected human monocyte-derived macrophages and dendritic cells. Of the 12 chemokines analyzed, mRNAs for two, CXCL10 and CXCL11, ligands for the chemokine receptor CXCR3, were up-regulated in both cell types upon infection by HIV-1. Induction of these chemokine genes in infected cultures was dependent on both viral entry and reverse transcriptase activity, but not on the HIV-1 envelope glycoprotein. Conditioned medium from infected cells was chemotactic for freshly isolated human CD4+ T cells, and chemotaxis was abolished by pretreatment with an Ab against CXCR3. A lymph node from an HIV-1-infected individual expressed CXCL10 and CXCL11 mRNAs in the paracortex, including venules, as detected by in situ hybridization, whereas neither mRNA was detected after highly active antiretroviral therapy. Because CCR5 on CD4+ T cells is found predominantly on cells that also express CXCR3, these data implicate CXCL10 and CXCL11 in the recruitment of susceptible T cells to HIV-1-infected lymph nodes, macrophages, and dendritic cells. This recruitment might enhance the sequestration of T cells in infected lymphoid organs and the spread of infection between cells, contributing to the immunopathology of AIDS.

show abstract

“…In contrast to the Cxcl9 gene, both IFN-␥-dependent and -independent pathways mediate expression of the Cxcl10 gene in LCM. Indeed, it has been shown previously that other cytokines such as type I interferons (IFNs) and TNF-␣ (30,31,35,36), as well as microbial products such as LPS and HIV gp120 (4,31) ferences in the regulation of Cxcl9 and Cxcl10 gene expression can best be explained by differences in the promoters for both genes that contain distinct transcription factor binding sites (17,32,44).…”

Section: Discussionmentioning

confidence: 99%

Unaltered Neurological Disease and Mortality in CXCR3-Deficient Mice Infected Intracranially with Lymphocytic Choriomeningitis Virus-Armstrong

et al. 2008

Self Cite

View full text Add to dashboard Cite

Intracranial infection of mice with lymphocytic choriomeningitis virus (LCMV) results in a lethal neurological disease termed lymphocytic choriomeningitis (LCM) that is mediated by antiviral CD8 ϩ T cells. Previous studies have implicated the chemokine receptor CXCR3 and its ligand CXCL10 in CD8 ϩ T cell trafficking in the brain and in the lethal disease following intracranial infection of mice with the LCMV-Traub strain. Here we investigated the role of CXCR3 in LCM following intracranial infection of mice with the LCMV-Armstrong strain. Significant induction of both CXCL9 and CXCL10 RNA and protein was seen in the central nervous system (CNS) in LCM. Cellular localization of the CXCL9 and CXCL10 RNA transcripts was identified predominantly in infiltrating mononuclear cells, as well as in subpial and paraventricular microglia (CXCL9) and astrocytes (CXCL10). Despite a primary role of interferon (IFN)-␥ in inducing the expression of the CXCL9 gene, and to a lesser extent the CXCL10 gene in LCM, the absence of the IFN-␥ receptor did not influence the disease outcome. This finding suggested that these chemokines may not play a major role in the pathogenesis of LCM. To evaluate this possibility further the development of LCM was examined in mice that were deficient for CXCR3. Surprisingly, in the absence of CXCR3 there was no alteration in mortality, cytokine expression, or T cell infiltration in the CNS, demonstrating that in contrast to LCMV-Traub, CXCR3 is not involved in the pathogenesis of LCMV-Armstrong-induced neurological disease in mice. Our findings indicate that despite similar immunopathogenetic mechanisms involving antiviral CD8 ϩ T cells, whether or not CXCR3 signaling has a role in LCM is dependent upon the infecting strain of LCMV. 425

show abstract

Interferon-Independent, Human Immunodeficiency Virus Type 1 gp120-Mediated Induction of CXCL10/IP-10 Gene Expression by Astrocytes In Vivo and In Vitro

Cited by 122 publications

References 68 publications

Role of Interleukin-1 in Prion Disease-Associated Astrocyte Activation

Role of Interleukin-1 in Prion Disease-Associated Astrocyte Activation

Roles for CXC Chemokine Ligands 10 and 11 in Recruiting CD4+ T Cells to HIV-1-Infected Monocyte-Derived Macrophages, Dendritic Cells, and Lymph Nodes

Unaltered Neurological Disease and Mortality in CXCR3-Deficient Mice Infected Intracranially with Lymphocytic Choriomeningitis Virus-Armstrong

Contact Info

Product

Resources

About