Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-11-8
pubmed:abstractText
Disease progression in HIV-1 infection is reported to be associated with a gradual shift in CD4+ T cell function from a Th type 1 to a Th type 2 of response, but the underlying mechanism remains unclear. In this study, the effect of HIV-1 envelope glycoprotein gp160 on secretion of cytokines IFN-gamma/IL-2 (Th1 type) and IL-4 (Th2 type) was analyzed using freshly isolated unfractioned peripheral blood mononuclear cells (PBMC), CD4+ T cell lines, and PBMC depleted of CD8+ cells (CD8- PBMC) as target cells. Pretreatment of these cells with HIV gp160 significantly reduced PHA-induced secretion of IFN-gamma and IL-2 but augmented IL-4 production. This effect of gp160 was not observed when the target cells consisted of PBMC depleted of either CD4+ cells (CD4- PBMC) or of CD2+ cells (CD2- PBMC). Pretreatment of gp160 with soluble CD4-immunoglobulin chimeric molecules abrogated the observed effects of gp160, suggesting that CD4-gp120 interaction is required for modification of the cytokine secretion profile. Our results suggest that exposure of CD4+ T cells to HIV-1 envelope proteins may modify the responses evoked by additional stimuli in favor of a Th2-type dominant response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0090-1229
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
245-51
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
HIV-1 gp160 as a modifier of Th1 and Th2 cytokine response: gp160 suppresses interferon-gamma and interleukin-2 production concomitantly with enhanced interleukin-4 production in vitro.
pubmed:affiliation
Department of Pediatrics, North Shore University Hospital-Cornell University Medical College, Manhasset, New York, New York 11030.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.