pubmed-article:7907660 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7907660 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:7907660 | lifeskim:mentions | umls-concept:C0241526 | lld:lifeskim |
pubmed-article:7907660 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:7907660 | lifeskim:mentions | umls-concept:C1291802 | lld:lifeskim |
pubmed-article:7907660 | lifeskim:mentions | umls-concept:C0205100 | lld:lifeskim |
pubmed-article:7907660 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:7907660 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:7907660 | pubmed:dateCreated | 1994-4-21 | lld:pubmed |
pubmed-article:7907660 | pubmed:abstractText | Human immunodeficiency virus type 1 (HIV-1) gp-120 potentially plays an important role in inducing functional suppression and depletion of CD4 lymphocytes following infection with HIV. In order to further understand the mechanisms involved in HIV-induced immunosuppression, we have studied the effects of recombinant HIV-1 gp120/SF2 and anti-gp120/SF2 antibodies on T cell receptor (TCR)-mediated proliferation of peripheral blood mononuclear cells (PBMCs) and isolated lymphocyte subsets from HIV-seronegative donors. In a dose-dependent manner, gp120 significantly reduces the proliferative responses of unfractionated PBMCs and highly enriched CD4 T lymphocytes when they are polyclonally stimulated through the TCR using WT31 (anti-alpha beta Ti chains) and anti-Leu 4 (anti-CD3 epsilon) in the presence of autologous accessory cells. The addition of divalent anti-gp120/SF2 to lymphocytes previously incubated with gp120 further reduces the proliferation to the levels seen after pretreating cells with divalent anti-CD4 (anti-Leu 3a). CD8 T lymphocytes, on the other hand, show no change in TCR-mediated proliferation following preincubation with either anti-CD4 or gp120/anti-gp120. We find no evidence for significant cell death by apoptosis using methods of DNA analysis or flow cytometry and DNA-specific dyes to account for the loss of CD4 lymphocyte proliferation. Interleukin-2 restores the proliferation suppressed by gp120/anti-gp120 suggesting the induction of reversible functional anergy. | lld:pubmed |
pubmed-article:7907660 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:language | eng | lld:pubmed |
pubmed-article:7907660 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7907660 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:7907660 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7907660 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7907660 | pubmed:month | Apr | lld:pubmed |
pubmed-article:7907660 | pubmed:issn | 0894-9255 | lld:pubmed |
pubmed-article:7907660 | pubmed:author | pubmed-author:StitesD PDP | lld:pubmed |
pubmed-article:7907660 | pubmed:author | pubmed-author:LieglerT JTJ | lld:pubmed |
pubmed-article:7907660 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7907660 | pubmed:volume | 7 | lld:pubmed |
pubmed-article:7907660 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7907660 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7907660 | pubmed:pagination | 340-8 | lld:pubmed |
pubmed-article:7907660 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:7907660 | pubmed:meshHeading | pubmed-meshheading:7907660-... | lld:pubmed |
pubmed-article:7907660 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7907660 | pubmed:articleTitle | HIV-1 gp120 and anti-gp120 induce reversible unresponsiveness in peripheral CD4 T lymphocytes. | lld:pubmed |
pubmed-article:7907660 | pubmed:affiliation | Department of Laboratory Medicine, University of California, San Francisco. | lld:pubmed |
pubmed-article:7907660 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7907660 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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