pubmed-article:8102328 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C0205148 | lld:lifeskim |
pubmed-article:8102328 | lifeskim:mentions | umls-concept:C1704241 | lld:lifeskim |
pubmed-article:8102328 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:8102328 | pubmed:dateCreated | 1993-9-10 | lld:pubmed |
pubmed-article:8102328 | pubmed:abstractText | The mechanism of CD4+ cell depletion and functional T helper cell inhibition in HIV-infected individuals is poorly understood. The present study demonstrates that immune complex-covered CD4+ cells are associated with T cell inhibition and macrophage stimulation. We studied 30 patients with ARC/AIDS and 35 asymptomatic HIV+ haemophilia patients. Overall, 20 +/- 3% of peripheral CD4+ lymphocytes were covered with gp120 (range 0-94%). gp120+ cells also exhibited surface-bound IgG (P = 0.0001), IgM (P = 0.0001), and complement (P = 0.0001). Decreased in vitro lymphocyte proliferation was associated with the immune complex load of CD4+ cells. The higher the percentage of CD4+ gp 120+ cells in the blood, the lower the T cell response in vitro (P = 0.001). Moreover, an association was found between immune complex-positive cells and plasma neopterin (P = 0.01). Patients with increased plasma neopterin levels had decreased in vitro responses to pokeweed mitogen (PWM) (P = 0.006), phytohaemagglutinin (PHA) (P = 0.004), concanavalin A (Con A) (P = 0.09), and anti-CD3 MoAb (P = 0.03), and decreased CD4+ cell counts in the blood (P = 0.006). Since maximally 1% of CD4+ lymphocytes are infected with HIV, T cell dysfunction and T cell depletion in HIV-infected patients may also be caused by the release of free gp120 that binds to uninfected CD4+ cells. Our data suggest that the functional inhibition and subsequent elimination of uninfected CD4+ lymphocytes with surface gp120-immunoglobulin-complement complexes may be a pathomechanism in the manifestation of AIDS. | lld:pubmed |
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pubmed-article:8102328 | pubmed:language | eng | lld:pubmed |
pubmed-article:8102328 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8102328 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8102328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8102328 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8102328 | pubmed:month | Aug | lld:pubmed |
pubmed-article:8102328 | pubmed:issn | 0009-9104 | lld:pubmed |
pubmed-article:8102328 | pubmed:author | pubmed-author:OpelzGG | lld:pubmed |
pubmed-article:8102328 | pubmed:author | pubmed-author:ZimmermannRR | lld:pubmed |
pubmed-article:8102328 | pubmed:author | pubmed-author:DanielVV | lld:pubmed |
pubmed-article:8102328 | pubmed:author | pubmed-author:SüsalCC | lld:pubmed |
pubmed-article:8102328 | pubmed:author | pubmed-author:WeimerRR | lld:pubmed |
pubmed-article:8102328 | pubmed:author | pubmed-author:Huth-KühneAA | lld:pubmed |
pubmed-article:8102328 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8102328 | pubmed:volume | 93 | lld:pubmed |
pubmed-article:8102328 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8102328 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8102328 | pubmed:pagination | 152-6 | lld:pubmed |
pubmed-article:8102328 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8102328 | pubmed:meshHeading | pubmed-meshheading:8102328-... | lld:pubmed |
pubmed-article:8102328 | pubmed:year | 1993 | lld:pubmed |
pubmed-article:8102328 | pubmed:articleTitle | Association of T cell and macrophage dysfunction with surface gp 120-immunoglobulin-complement complexes in HIV-infected patients. | lld:pubmed |
pubmed-article:8102328 | pubmed:affiliation | Department of Transplantation Immunology, University of Heidelberg, Germany. | lld:pubmed |
pubmed-article:8102328 | pubmed:publicationType | Journal Article | lld:pubmed |
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