Linked Life Data

14734774

Source:http://linkedlifedata.com/resource/pubmed/id/14734774

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-1-21
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
172
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1888-95
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:14734774-Amino Acid Motifs, pubmed-meshheading:14734774-Animals, pubmed-meshheading:14734774-Astrocytes, pubmed-meshheading:14734774-Brain, pubmed-meshheading:14734774-Cell Line, Tumor, pubmed-meshheading:14734774-Cells, Cultured, pubmed-meshheading:14734774-Chemokines, C, pubmed-meshheading:14734774-Gene Expression Regulation, pubmed-meshheading:14734774-Gene Products, tat, pubmed-meshheading:14734774-HIV-1, pubmed-meshheading:14734774-Humans, pubmed-meshheading:14734774-Lymphocyte Activation, pubmed-meshheading:14734774-Lymphokines, pubmed-meshheading:14734774-Macrophages, pubmed-meshheading:14734774-Mice, pubmed-meshheading:14734774-Mice, Transgenic, pubmed-meshheading:14734774-Microglia, pubmed-meshheading:14734774-Monocytes, pubmed-meshheading:14734774-Promoter Regions, Genetic, pubmed-meshheading:14734774-RNA, Messenger, pubmed-meshheading:14734774-Sialoglycoproteins, pubmed-meshheading:14734774-T-Lymphocytes, pubmed-meshheading:14734774-Up-Regulation, pubmed-meshheading:14734774-tat Gene Products, Human Immunodeficiency Virus
pubmed:year
2004
pubmed:articleTitle
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.
pubmed:affiliation
Department of Microbiology and Immunology, Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't