| http://purl.uniprot.org/citations/14734774 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/14734774 | http://www.w3.org/2000/01/rdf-schema#comment | "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-1alpha (MIP-1alpha)), CCL4 (MIP-1beta), CCL5 (RANTES), CXCL2 (MIP-2), and CXCL10 (inducing protein-10), XCL1 (lymphotactin/single C motif-1alpha/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."xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.172.3.1888"xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/author | "He J.J."xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/author | "Kim B.O."xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/author | "Zhou B.Y."xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/pages | "1888-1895"xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/title | "Induction of C chemokine XCL1 (lymphotactin/single C motif-1 alpha/activation-induced, T cell-derived and chemokine-related cytokine) expression by HIV-1 Tat protein."xsd:string |
| http://purl.uniprot.org/citations/14734774 | http://purl.uniprot.org/core/volume | "172"xsd:string |
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