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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0021747,
umls-concept:C0021758,
umls-concept:C0021764,
umls-concept:C0022688,
umls-concept:C0024264,
umls-concept:C0035253,
umls-concept:C0036667,
umls-concept:C0086418,
umls-concept:C0108779,
umls-concept:C0108800,
umls-concept:C0185117,
umls-concept:C0312418,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
1992-6-11
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pubmed:abstractText |
The effect of rIL-4 on CD69 antigen expression induced by rIL-2 or by rINF-alpha on human resting NK cells and CD3+, CD4-, CD8- T lymphocytes has been investigated. rIL-4 drastically inhibited CD69 antigen expression induced by rIL-2 in both cell types. In contrast, rIL-4 did not alter rINF-alpha-induced CD69 antigen expression. Consistent results were obtained evaluating the cytolytic activity of NK cells against the Raji target cell line: rINF-alpha-induced lytic activity was not inhibited by rIL-4, while rIL-2-induced lytic activity was drastically inhibited. Proliferative activity of NK cells induced by rIL-2, in contrast, was only slightly reduced by rIL-4. rIL-4 did not alter the expression of the beta chain of IL-2 receptor, evaluated in NK cells by indirect immunofluorescence. Expression of the alpha chain of IL-2 receptor could not be detected in NK cells by indirect immunofluorescence. It can therefore be suggested that the selective inhibitory effect of rIL-4 on rIL-2-induced activation of NK cells is not mediated by downregulation of alpha and beta chains of IL-2 receptor.
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0008-8749
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
141
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
342-51
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:1533569-Antigens, CD,
pubmed-meshheading:1533569-Antigens, CD3,
pubmed-meshheading:1533569-Antigens, CD4,
pubmed-meshheading:1533569-Antigens, CD8,
pubmed-meshheading:1533569-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:1533569-Gene Expression Regulation,
pubmed-meshheading:1533569-Humans,
pubmed-meshheading:1533569-Interferon-alpha,
pubmed-meshheading:1533569-Interleukin-2,
pubmed-meshheading:1533569-Interleukin-4,
pubmed-meshheading:1533569-Killer Cells, Natural,
pubmed-meshheading:1533569-Lectins, C-Type,
pubmed-meshheading:1533569-Lymphocyte Subsets,
pubmed-meshheading:1533569-Receptors, Antigen, T-Cell,
pubmed-meshheading:1533569-Recombinant Proteins
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pubmed:year |
1992
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pubmed:articleTitle |
Different sensitivity to interleukin 4 of interleukin 2- and interferon alpha-induced CD69 antigen expression in human resting NK cells and CD3+, CD4-, CD8- lymphocytes.
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pubmed:affiliation |
Istituto di Scienze Immunologiche, Università di Verona, Italy.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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