Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-2-9
pubmed:abstractText
Interleukin 21 exerts a variety of regulatory effects on both innate and adaptive immune cells. Although the suppressive effect of IL-21 via the induction of IL-10 in mouse model has been defined, the inhibitory effect of IL-21 in humans is not well understood. In the present study, we showed that IL-21 induced IL-10 production by human naive CD4(+) T cells. Most of the IL-10-producing CD4(+) T cells did not co-express IFN-?. IL-21 increased the expression of IL-21R on activated naïve CD4(+) T cells. Further analysis indicated that IL-21 induced phosphorylation of STAT1, STAT3 and STAT5 in activated naïve CD4(+) T cells. In addition, IL-21 maintained the expression of CD16 on monocytes via the production of IL-10 by human naïve CD4(+) T cells. Taken together, our data indicated that IL-21 had a modulating effect on monocytes at least in part by inducing IL-10 production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3, http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Conditioned, http://linkedlifedata.com/resource/pubmed/chemical/FCGR3B protein, human, http://linkedlifedata.com/resource/pubmed/chemical/GPI-Linked Proteins, http://linkedlifedata.com/resource/pubmed/chemical/HLA-DR Antigens, http://linkedlifedata.com/resource/pubmed/chemical/IL10 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/IL21R protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-21 Receptor alpha..., http://linkedlifedata.com/resource/pubmed/chemical/Interleukins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG, http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/STAT5 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/interleukin-21
pubmed:status
MEDLINE
pubmed:issn
1090-2163
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
267
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
102-8
pubmed:meshHeading
pubmed-meshheading:21227406-Antibodies, pubmed-meshheading:21227406-Antigens, CD28, pubmed-meshheading:21227406-Antigens, CD3, pubmed-meshheading:21227406-CD4-Positive T-Lymphocytes, pubmed-meshheading:21227406-Culture Media, Conditioned, pubmed-meshheading:21227406-Fetal Blood, pubmed-meshheading:21227406-GPI-Linked Proteins, pubmed-meshheading:21227406-HLA-DR Antigens, pubmed-meshheading:21227406-Humans, pubmed-meshheading:21227406-Interferon-gamma, pubmed-meshheading:21227406-Interleukin-10, pubmed-meshheading:21227406-Interleukin-21 Receptor alpha Subunit, pubmed-meshheading:21227406-Interleukins, pubmed-meshheading:21227406-Leukocytes, Mononuclear, pubmed-meshheading:21227406-Lymphocyte Activation, pubmed-meshheading:21227406-Monocytes, pubmed-meshheading:21227406-Phosphorylation, pubmed-meshheading:21227406-Receptors, IgG, pubmed-meshheading:21227406-STAT1 Transcription Factor, pubmed-meshheading:21227406-STAT3 Transcription Factor, pubmed-meshheading:21227406-STAT5 Transcription Factor
pubmed:year
2011
pubmed:articleTitle
Interleukin-21 maintains the expression of CD16 on monocytes via the production of IL-10 by human naïve CD4+ T cells.
pubmed:affiliation
Department of Immunology, Zhongshan School of Medicine, Key Laboratory of Tropical Disease Control Research of Ministry of Education, Sun Yat-sen University, Guangzhou, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't