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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0003873,
umls-concept:C0014644,
umls-concept:C0021311,
umls-concept:C0021745,
umls-concept:C0021755,
umls-concept:C0021756,
umls-concept:C0024297,
umls-concept:C0030685,
umls-concept:C0033268,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1533691,
umls-concept:C1963578,
umls-concept:C1999216
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pubmed:issue |
10
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pubmed:dateCreated |
1986-6-6
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pubmed:abstractText |
Epstein Barr virus (EBV)-infection of normal peripheral blood mononuclear cells (PBMC) in vitro induces IFN-alpha secretion from B cell and natural killer (NK) cell populations, and IFN-gamma secretion from T cells. IFN-gamma depends on prior elaboration of IL 2 and IL 1 that originates from monocytes and NK cells. PBMC from rheumatoid arthritis (RA) patients released moderately elevated levels of IFN-alpha (236 +/- 62 U/ml vs 168 +/- 34 in normals). In contrast, IFN-gamma was significantly lower in RA (88 +/- 34 U/ml vs 209 +/- 32) with an associated deficit in IL 2. A monocyte-dependent factor was shown to be responsible for this deficit, since monocyte depletion of RA cultures normalized the levels of IL 2 and IFN-gamma. Significantly lower levels of IL 1 activity were present in the supernatants of RA PBMC cultures as compared with normal cultures, and this was shown to be associated with presence of a nondialyzable IL 1 inhibitor. This inhibitor was capable of preventing the IL 1-dependent synthesis of IL 2 and IFN-gamma by normal PBMC. Exogenous IL 1 or IL 2 restored the deficient IFN-gamma secretion in RA PBMC. Thus, the deficient ability of RA lymphocytes to control EBV infection may be secondary to impairment of a monocyte-T cell interaction at the level of IL 1.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
136
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3643-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:3009609-Adult,
pubmed-meshheading:3009609-Aged,
pubmed-meshheading:3009609-Arthritis, Rheumatoid,
pubmed-meshheading:3009609-Cells, Cultured,
pubmed-meshheading:3009609-Female,
pubmed-meshheading:3009609-Herpesviridae Infections,
pubmed-meshheading:3009609-Herpesvirus 4, Human,
pubmed-meshheading:3009609-Humans,
pubmed-meshheading:3009609-Interferon Type I,
pubmed-meshheading:3009609-Interferon-gamma,
pubmed-meshheading:3009609-Interleukin-1,
pubmed-meshheading:3009609-Interleukin-2,
pubmed-meshheading:3009609-Lymphocytes,
pubmed-meshheading:3009609-Lymphokines,
pubmed-meshheading:3009609-Male,
pubmed-meshheading:3009609-Middle Aged,
pubmed-meshheading:3009609-Monocytes,
pubmed-meshheading:3009609-Time Factors
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pubmed:year |
1986
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pubmed:articleTitle |
Release of lymphokines after infection with Epstein Barr virus in vitro. II. A monocyte-dependent inhibitor of interleukin 1 downregulates the production of interleukin 2 and interferon-gamma in rheumatoid arthritis.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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