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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-6-28
pubmed:abstractText
Dendritic cells (DC) and macrophages play an important role in the generation of immune responses and transmission of HIV infection. It has been recently found that, in the presence of gp120, CD4 can be efficiently coimmunoprecipitated by anti-CXCR4 antibodies from lymphocytes and monocytes but not from blood monocyte-derived macrophages. The gp120-CD4-CXCR4 complex formation paralleled the ability for these cell types to support X4 (LAV) HIV-1 envelope glycoprotein (Env)-mediated fusion. Here we report that, unlike macrophages but similar to lymphocytes and monocytes, human blood monocyte-derived DC allow efficient complex formation among the HIV-1 coreceptor CXCR4, the primary receptor CD4, and the Env gp120 (LAV) which parallels their fusion ability with cells expressing HIV-1 Env (LAV). In addition, DC behaved similarly to macrophages, lymphocytes, and monocytes in their ability to support formation of complexes between CD4 and the other major HIV-1 coreceptor CCR5 even in the absence of gp120 as demonstrated by CD4 coimmunoprecipitation with anti-CCR5 antibodies. Further, the amount of gp120-CD4-CXCR4 (or CCR5) complexes was proportional to the extent of cell fusion mediated by the HIV-1 Env (LAV or JRFL, respectively). These results demonstrate that of all the major types of host cells important for HIV-1 infection, the first central stage in the entry mechanism, the formation of gp120-CD4-coreceptor complexes, is not impaired except for the formation of the gp120-CD4-CXCR4 complex in macrophages. Therefore, for most CD4+ target cells restraint(s) on productive HIV-1 infection appears to occur at stages of the virus life cycle subsequent to the gp120-CD4-coreceptor complex formation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-4800
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10816381-Animals, pubmed-meshheading:10816381-Antigens, CD4, pubmed-meshheading:10816381-Cell Differentiation, pubmed-meshheading:10816381-Cell Fusion, pubmed-meshheading:10816381-Cell Line, pubmed-meshheading:10816381-Cercopithecus aethiops, pubmed-meshheading:10816381-Dendritic Cells, pubmed-meshheading:10816381-Flow Cytometry, pubmed-meshheading:10816381-Genes, env, pubmed-meshheading:10816381-Genetic Vectors, pubmed-meshheading:10816381-HIV Envelope Protein gp120, pubmed-meshheading:10816381-HIV-1, pubmed-meshheading:10816381-Humans, pubmed-meshheading:10816381-Macromolecular Substances, pubmed-meshheading:10816381-Monocytes, pubmed-meshheading:10816381-Receptors, CCR5, pubmed-meshheading:10816381-Receptors, CXCR4, pubmed-meshheading:10816381-Recombinant Fusion Proteins, pubmed-meshheading:10816381-Vaccinia virus
pubmed:year
2000
pubmed:articleTitle
Interactions of CCR5 and CXCR4 with CD4 and gp120 in human blood monocyte-derived dendritic cells.
pubmed:affiliation
Laboratory of Experimental and Computational Biology, NCI-FCRDC, NIH, Frederick, Maryland, 21702-1201, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.