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rdf:type |
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lifeskim:mentions |
umls-concept:C0003209,
umls-concept:C0019682,
umls-concept:C0019699,
umls-concept:C0021758,
umls-concept:C0026473,
umls-concept:C0085732,
umls-concept:C0128546,
umls-concept:C0254610,
umls-concept:C0441655,
umls-concept:C1422055,
umls-concept:C1515999,
umls-concept:C1522012,
umls-concept:C1555029,
umls-concept:C1948023
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pubmed:issue |
1-2
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pubmed:dateCreated |
2006-4-24
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pubmed:abstractText |
Monocytes play a central role in the immune system by producing and reacting to different soluble factors. Cytokine dysregulation is an hallmark in HIV-infected individuals and it is one of the most significant factors leading to impaired immunity in HIV/AIDS disease. This study investigates the possibility of modulation in the secretion of some inflammatory cytokines and chemokines induced by HIV p17 in monocytes. The results show that p17, while ineffective on resting monocytes, exerts an inflammatory action on IL-4 mediated inhibition of TNF-alpha and IFN-gamma production induced by IL-15 stimulation. In addition, p17 is able to reduce MIP-1alpha secretion, but unable to influence IL-6 production. The ability of HIV p17 to contribute to an altered pattern of secreted soluble factors might imply a key role for this viral protein in the development of AIDS pathogenesis.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, gag,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-15,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/gag Gene Products, Human...,
http://linkedlifedata.com/resource/pubmed/chemical/p17 protein, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0168-1702
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
118
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
170-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16427155-Animals,
pubmed-meshheading:16427155-Chemokine CCL3,
pubmed-meshheading:16427155-Chemokine CCL4,
pubmed-meshheading:16427155-Gene Products, gag,
pubmed-meshheading:16427155-HIV Antigens,
pubmed-meshheading:16427155-HIV-1,
pubmed-meshheading:16427155-Humans,
pubmed-meshheading:16427155-Interferon-gamma,
pubmed-meshheading:16427155-Interleukin-15,
pubmed-meshheading:16427155-Interleukin-4,
pubmed-meshheading:16427155-Interleukin-6,
pubmed-meshheading:16427155-Macrophage Inflammatory Proteins,
pubmed-meshheading:16427155-Mice,
pubmed-meshheading:16427155-Monocytes,
pubmed-meshheading:16427155-Tumor Necrosis Factor-alpha,
pubmed-meshheading:16427155-Viral Proteins,
pubmed-meshheading:16427155-gag Gene Products, Human Immunodeficiency Virus
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pubmed:year |
2006
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pubmed:articleTitle |
HIV p17 reverses the anti-inflammatory activity of IL-4 on IL-15 stimulated monocytes and modulates their ability to secrete MIP-1 alpha.
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pubmed:affiliation |
Institute of Microbiology and Virology, University of Brescia, Brescia, Italy. defrance@med.unibs.it
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pubmed:publicationType |
Journal Article
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