Source:http://linkedlifedata.com/resource/pubmed/id/17947662
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0032112,
umls-concept:C0035820,
umls-concept:C0079411,
umls-concept:C0205224,
umls-concept:C0282116,
umls-concept:C0962190,
umls-concept:C1149231,
umls-concept:C1155003,
umls-concept:C1332714,
umls-concept:C1334107,
umls-concept:C1367171,
umls-concept:C1416406,
umls-concept:C1423038,
umls-concept:C1831593
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pubmed:issue |
9
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pubmed:dateCreated |
2007-10-19
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pubmed:abstractText |
During T cell-B cell collaboration, plasma cell (PC) differentiation and Ig production are known to require T cell-derived soluble factors. However, the exact nature of the cytokines produced by activated T cells that costimulate PC differentiation is not clear. Previously, we reported that costimulation of purified human B cells with IL-21 and anti-CD40 resulted in efficient PC differentiation. In this study, we addressed whether de novo production of IL-21 was involved in direct T cell-induced B cell activation, proliferation, and PC differentiation. We found that activated human peripheral blood CD4(+) T cells expressed mRNA for a number of cytokines, including IL-21, which was confirmed at the protein level. Using a panel of reagents that specifically neutralize cytokine activity, we addressed which cytokines are essential for B cell activation and PC differentiation induced by anti-CD3-activated T cells. Strikingly, neutralization of IL-21 with an IL-21R fusion protein (IL-21R-Fc) significantly inhibited T cell-induced B cell activation, proliferation, PC differentiation, and Ig production. Inhibition of PC differentiation was observed even when the addition of IL-21R-Fc was delayed until after initial B cell activation and expansion had occurred. Importantly, IL-21 was found to be involved in PC differentiation from both naive and memory B cells. Finally, IL-21R-Fc did not inhibit anti-CD3-induced CD4(+) T cell activation, but rather directly blocked T cell-induced B cell activation and PC differentiation. These data are the first to document that B cell activation, expansion, and PC differentiation induced by direct interaction of B cells with activated T cells requires IL-21.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
179
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5886-96
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17947662-Antibodies,
pubmed-meshheading:17947662-Antigens, CD3,
pubmed-meshheading:17947662-B-Lymphocytes,
pubmed-meshheading:17947662-CD4-Positive T-Lymphocytes,
pubmed-meshheading:17947662-Cell Differentiation,
pubmed-meshheading:17947662-Cell Proliferation,
pubmed-meshheading:17947662-Cells, Cultured,
pubmed-meshheading:17947662-Humans,
pubmed-meshheading:17947662-Immunity, Innate,
pubmed-meshheading:17947662-Immunologic Memory,
pubmed-meshheading:17947662-Interleukins,
pubmed-meshheading:17947662-Lymphocyte Activation,
pubmed-meshheading:17947662-Plasma Cells
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pubmed:year |
2007
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pubmed:articleTitle |
Essential role of IL-21 in B cell activation, expansion, and plasma cell generation during CD4+ T cell-B cell collaboration.
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pubmed:affiliation |
Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Intramural
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