rdf:type |
|
lifeskim:mentions |
umls-concept:C0019682,
umls-concept:C0021469,
umls-concept:C0021755,
umls-concept:C0024432,
umls-concept:C0030685,
umls-concept:C0086418,
umls-concept:C0391871,
umls-concept:C0441655,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1515655,
umls-concept:C1533691,
umls-concept:C1963578
|
pubmed:issue |
6
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pubmed:dateCreated |
1989-1-20
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pubmed:abstractText |
Infection of monocyte-macrophages with human immunodeficiency virus may be central to the pathogenesis of the acquired immunodeficiency syndrome. The ability of infected macrophages to prime T cells through IL-1 production was investigated in vitro. Purified human monocytes maintained in suspension culture were infected with strain HIV-DV. Intracellular expression of virus p24 antigen increased from undetectable levels immediately after infection to 13-59% of cells by 10-14 d; infected macrophages remained viable for up to 60 d. Supernatants collected between 14 and 20 d after infection were examined in the murine thymocyte co-mitogenesis assay and demonstrated to contain a potent IL-1 inhibitor, designated contra-IL-1. Contra-IL-1 activity was present in all supernatants examined after 4 d of infection, and peaked coincident with peak p24 antigen expression. Inhibitory activity was not present in uninfected cells. Contra-IL-1 activity eluted after gel filtration with an approximate molecular weight of 9 kD. Inhibitory activity was removed by exposure to heat or acid pH, or by incubation with chymotrypsin or staphylococcal V8 protease. Contra-IL-1 did not inhibit IL-2- or IL-4-dependent proliferation of murine T cell lines. Despite its ability to inhibit IL-1 activity, contra-IL-1 did not interfere with the binding of recombinant IL-1 beta to a fibroblast cell line. Contra-IL-1 inhibited the proliferation of normal peripheral blood mononuclear cells to both concanavalin A and tetanus toxoid; inhibition could be attenuated by the addition of exogenous IL-1. Messenger RNA extracted from infected macrophages was examined by Northern analysis for the presence of message to IL-1 beta. No message was apparent, suggesting that the presence of contra-IL-1 was not obscuring the concomitant release of IL-1. Infected macrophages stimulated with endotoxin generated readily detectable message for IL-1 beta. Spleen macrophages purified from two patients with AIDS complicated by immune thrombocytopenia spontaneously expressed p24 antigen in vitro and released contra-IL-1 activity into the media. Contra-IL-1 may contribute to the immune dysfunction of AIDS.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/3264291-2415141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3264291-2419430,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/3264291-6795276,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3264291-92524
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0021-9738
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
82
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pubmed:owner |
NLM
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