Source:http://linkedlifedata.com/resource/pubmed/id/10671214
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rdf:type | |
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0019704,
umls-concept:C0039194,
umls-concept:C0085732,
umls-concept:C0183683,
umls-concept:C0185117,
umls-concept:C0205245,
umls-concept:C0344211,
umls-concept:C0598312,
umls-concept:C0871161,
umls-concept:C1171411,
umls-concept:C1317973,
umls-concept:C1332714,
umls-concept:C1413236,
umls-concept:C1515021,
umls-concept:C1521721,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2000-3-14
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pubmed:abstractText |
Enrichment of a subset of CD4(+)CD45R0(+)CD7(-) T cells has been observed in HIV-infected individuals. We have investigated the ability of CD7(+) and CD7(-) T cells to support replication of HIV and show that virus replicates preferentially in CD7(+) cells. Several possible mechanisms that may underlie such differences in susceptibility to HIV were studied. Our data demonstrate that mitogen stimulation induces poor expression of CD25 and IL-2 in CD7(-) compared with CD7(+) cells. We also show that uninfected CD7(-) cells are more resistant to mitogen-induced apoptosis than CD7(+) cells. Our data support the view that the CD7(-) subset is inherently resistant to HIV replication and that this is due in part to reduced CD25 expression and IL-2 production.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
577-85
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10671214-Acquired Immunodeficiency Syndrome,
pubmed-meshheading:10671214-Antigens, CD7,
pubmed-meshheading:10671214-CD4-Positive T-Lymphocytes,
pubmed-meshheading:10671214-Disease Susceptibility,
pubmed-meshheading:10671214-HIV-1,
pubmed-meshheading:10671214-Humans,
pubmed-meshheading:10671214-Virus Replication
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pubmed:year |
2000
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pubmed:articleTitle |
CD7 expression distinguishes subsets of CD4(+) T cells with distinct functional properties and ability to support replication of HIV-1.
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pubmed:affiliation |
Edward Jenner Institute for Vaccine Research, Compton, GB. diana.wallace@jenner.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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