Linked Life Data

2576928

Source:http://linkedlifedata.com/resource/pubmed/id/2576928

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1990-7-27
pubmed:abstractText
To identify mechanisms which might facilitate emigration of HIV-1-infected cells from the circulation, we studied the effect of HIV-1 infection on T lymphocyte and monocytoid cell expression of molecules involved in adherence and translocation of leukocytes across endothelial cell barriers. CD11a, CD18, and ICAM-1 were demonstrated on up to 80% of HIV-1-infected H9 T cells by flow cytometry; these molecules were not evident on uninfected H9. CD18 mRNA was detected in HIV-infected, but not in uninfected H9 T cells. Cell surface expression of CD11a and CD18, but not ICAM-1, was increased on HIV-infected, as compared to uninfected U937 and THP1 monocytoid cells. Increased cell surface expression of the leukocyte integrins was associated with a significantly increased tendency of HIV-infected monocytoid cells to adhere to human umbilical vein endothelial cell monolayers or aggregate homotypically. Preincubating the monocytoid cells with anti-CD18 or anti-CD11a or preincubating endothelial cells with anti-ICAM-1 suppressed these cell to cell interactions. These studies suggest that HIV-1 infection stimulates cell surface expression of molecules involved in leukocyte adherence and transendothelial migration in vitro. Similar mechanisms may influence leukocyte trafficking, in vivo, and may play a role in the localization of HIV-1 infected cells in the central nervous system and other tissues.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0066-9458
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
117-30
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
HIV-1-stimulated expression of CD11/CD18 integrins and ICAM-1: a possible mechanism for extravascular dissemination of HIV-1-infected cells.
pubmed:affiliation
VA Medical Center, Houston, TX.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.