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rdf:type |
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lifeskim:mentions |
umls-concept:C0003209,
umls-concept:C0003320,
umls-concept:C0014653,
umls-concept:C0019682,
umls-concept:C0021756,
umls-concept:C0026926,
umls-concept:C0027361,
umls-concept:C0033684,
umls-concept:C0079189,
umls-concept:C0205227,
umls-concept:C0205263,
umls-concept:C0598312,
umls-concept:C0871261,
umls-concept:C1274040,
umls-concept:C1280500,
umls-concept:C1533691,
umls-concept:C1704632,
umls-concept:C1705180,
umls-concept:C1706817,
umls-concept:C1998793,
umls-concept:C2911692
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pubmed:issue |
5
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pubmed:dateCreated |
1998-5-29
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pubmed:abstractText |
Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is a serious problem, particularly in developing countries. Recently, M. tuberculosis and purified protein derivative (PPD) were demonstrated to induce HIV replication in CD8 T cell-depleted peripheral blood mononuclear cells from HIV-positive, PPD-positive persons but not in cells from PPD-negative persons. The role of endogenous and exogenous cytokines in modulating M. tuberculosis-induced HIV replication was evaluated. M. tuberculosis-induced HIV replication decreased following simultaneous inhibition of endogenous interleukin (IL)-2, IL-1beta, and tumor necrosis factor-alpha by the addition of soluble receptors and receptor antagonists or following exogenous IL-10 and transforming growth factor (TGF)-beta. In contrast, neutralization of endogenous IL-10 and TGF-beta augmented M. tuberculosis-induced HIV replication by increasing cellular activation. Thus, the balance between IL-2 and proinflammatory and antiinflammatory cytokines plays a major role in M. tuberculosis-induced replication of HIV.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1899
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
177
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1332-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:9593021-CD8-Positive T-Lymphocytes,
pubmed-meshheading:9593021-Cells, Cultured,
pubmed-meshheading:9593021-Cytokines,
pubmed-meshheading:9593021-HIV,
pubmed-meshheading:9593021-HIV Infections,
pubmed-meshheading:9593021-Humans,
pubmed-meshheading:9593021-Interferon-alpha,
pubmed-meshheading:9593021-Interferon-gamma,
pubmed-meshheading:9593021-Interleukins,
pubmed-meshheading:9593021-Lymphocyte Activation,
pubmed-meshheading:9593021-Lymphocyte Depletion,
pubmed-meshheading:9593021-Lymphocytes,
pubmed-meshheading:9593021-Mycobacterium tuberculosis,
pubmed-meshheading:9593021-Transforming Growth Factor beta,
pubmed-meshheading:9593021-Tuberculin,
pubmed-meshheading:9593021-Virus Replication
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pubmed:year |
1998
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pubmed:articleTitle |
The in vitro induction of human immunodeficiency virus (HIV) replication in purified protein derivative-positive HIV-infected persons by recall antigen response to Mycobacterium tuberculosis is the result of a balance of the effects of endogenous interleukin-2 and proinflammatory and antiinflammatory cytokines.
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pubmed:affiliation |
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-2520, USA.
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pubmed:publicationType |
Journal Article
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