| pubmed-article:7474110 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7474110 | lifeskim:mentions | umls-concept:C0019682 | lld:lifeskim |
| pubmed-article:7474110 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:7474110 | lifeskim:mentions | umls-concept:C0337611 | lld:lifeskim |
| pubmed-article:7474110 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:7474110 | lifeskim:mentions | umls-concept:C0039215 | lld:lifeskim |
| pubmed-article:7474110 | lifeskim:mentions | umls-concept:C0205250 | lld:lifeskim |
| pubmed-article:7474110 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:7474110 | pubmed:dateCreated | 1995-12-1 | lld:pubmed |
| pubmed-article:7474110 | pubmed:abstractText | Individuals infected with the human immunodeficiency virus (HIV) experience a marked loss of CD4+ T lymphocytes, leading to fatal immunodeficiency. The mechanisms causing the depletion of these cells are not yet understood. In this study, we observed that CD4+ T lymphocytes from HIV type 1 (HIV-1)-infected and uninfected individuals rapidly lysed B lymphoblasts expressing the HIV-1 envelope glycoprotein on the cell surface and Jurkat cells expressing the complete virus. Contact of uninfected CD4+ T cells with envelope glycoprotein-expressing cells also resulted in the lysis of the uninfected CD4+ T cells. Cytolysis did not require priming or in vitro stimulation of the CD4+ T cells and was not restricted by major histocompatibility complex molecules. Cytotoxicity was inhibited by soluble CD4 and anti-CD4 monoclonal antibodies that block binding of CD4 to gp120. In addition, neutralizing anti-CD4 and anti-gp120 monoclonal antibodies which block postbinding membrane fusion events and syncytium formation also inhibited cell lysis, suggesting that identical mechanisms in HIV-infected cultures underlie cell-cell fusion and the cytolysis observed. However, cytotoxicity was not always accompanied by the formation of visible syncytia. Rapid cell lysis after contact of uninfected and HIV-1-infected CD4+ T cells may explain CD4+ T-cell depletion in the absence of detectable syncytia in infected individuals. Moreover, because of its vigor, lysis of envelope-expressing targets by contact with unprimed CD4+ T lymphocytes may at first glance resemble antigen-specific immune responses and should be excluded when cytotoxic T-lymphocyte responses in infected individuals and vaccinees are evaluated. | lld:pubmed |
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| pubmed-article:7474110 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7474110 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7474110 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7474110 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7474110 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:7474110 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:7474110 | pubmed:author | pubmed-author:JassoyCC | lld:pubmed |
| pubmed-article:7474110 | pubmed:author | pubmed-author:SopperSS | lld:pubmed |
| pubmed-article:7474110 | pubmed:author | pubmed-author:HeinkeleinMM | lld:pubmed |
| pubmed-article:7474110 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7474110 | pubmed:volume | 69 | lld:pubmed |
| pubmed-article:7474110 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7474110 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7474110 | pubmed:pagination | 6925-31 | lld:pubmed |
| pubmed-article:7474110 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7474110 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7474110 | pubmed:articleTitle | Contact of human immunodeficiency virus type 1-infected and uninfected CD4+ T lymphocytes is highly cytolytic for both cells. | lld:pubmed |
| pubmed-article:7474110 | pubmed:affiliation | Institute for Virology and Immunobiology, Würzburg University, Germany. | lld:pubmed |
| pubmed-article:7474110 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7474110 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:7474110 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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