Source:http://linkedlifedata.com/resource/pubmed/id/10861047
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2000-7-31
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| pubmed:abstractText |
A 32-bp deletion in CCR5 (CCR5 Delta 32) confers to PBMC resistance to HIV-1 isolates that use CCR5 as a coreceptor. To study this mutation in T cell development, we have screened 571 human thymus tissues for the mutation. We identified 72 thymuses (12.6%) that were heterozygous and 2 (0.35%) that were homozygous for the CCR5 Delta 32 mutation. We found that thymocyte development was normal in both CCR5 Delta 32 heterozygous and homozygous thymuses. In 3% of thymuses we identified a functional polymorphism of CD45RA, in which cortical and medullary thymocytes failed to down-regulate the 200- and 220-kDa CD45RA isoforms during T cell development. Moreover, we found an association of this CD45 functional polymorphism in thymuses with the CCR5 Delta 32 mutation (p = 0.00258). In vitro HIV-1 infection assays with CCR5-using primary isolates demonstrated that thymocytes with the heterozygous CCR5 Delta 32 mutation produced less p24 than did CCR5 wild-type thymocytes. However, the functional CD45RA polymorphism did not alter the susceptibility of thymocytes to HIV-1 infection. Taken together, these data demonstrate association of the CCR5 Delta 32 mutation with a polymorphism in an as yet unknown gene that is responsible for the ability to down-regulate the expression of high m.w. CD45RA isoforms. Although the presence of the CCR5 Delta 32 mutation down-regulates HIV-1 infection of thymocytes, the functional CD45RA polymorphism does not alter the susceptibility of thymocytes to HIV-1 infection in vitro.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
165
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
148-57
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:10861047-Adolescent,
pubmed-meshheading:10861047-Adult,
pubmed-meshheading:10861047-Aged,
pubmed-meshheading:10861047-Aged, 80 and over,
pubmed-meshheading:10861047-Antigens, CD45,
pubmed-meshheading:10861047-Cells, Cultured,
pubmed-meshheading:10861047-Child,
pubmed-meshheading:10861047-Child, Preschool,
pubmed-meshheading:10861047-Genetic Linkage,
pubmed-meshheading:10861047-HIV Infections,
pubmed-meshheading:10861047-Humans,
pubmed-meshheading:10861047-Immunity, Innate,
pubmed-meshheading:10861047-Immunophenotyping,
pubmed-meshheading:10861047-Infant,
pubmed-meshheading:10861047-Infant, Newborn,
pubmed-meshheading:10861047-Leukocytes, Mononuclear,
pubmed-meshheading:10861047-Lymphocyte Subsets,
pubmed-meshheading:10861047-Middle Aged,
pubmed-meshheading:10861047-Mutation,
pubmed-meshheading:10861047-Organ Culture Techniques,
pubmed-meshheading:10861047-Polymorphism, Genetic,
pubmed-meshheading:10861047-Receptors, CCR5,
pubmed-meshheading:10861047-Thymus Gland
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| pubmed:year |
2000
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| pubmed:articleTitle |
Linkage of the CCR5 Delta 32 mutation with a functional polymorphism of CD45RA.
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| pubmed:affiliation |
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA. hliao@duke.edu'
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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