| pubmed-article:19620304 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19620304 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:19620304 | lifeskim:mentions | umls-concept:C0085295 | lld:lifeskim |
| pubmed-article:19620304 | lifeskim:mentions | umls-concept:C0439662 | lld:lifeskim |
| pubmed-article:19620304 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19620304 | pubmed:dateCreated | 2009-8-7 | lld:pubmed |
| pubmed-article:19620304 | pubmed:abstractText | IL-10 plays a central role in restraining the vigor of inflammatory responses, but the critical cellular sources of this counter-regulatory cytokine remain speculative in many disease models. Using a novel IL-10 transcriptional reporter mouse, we found an unexpected predominance of B cells (including plasma cells) among IL-10-expressing cells in peripheral lymphoid tissues at baseline and during diverse models of in vivo immunological challenge. Use of a novel B cell-specific IL-10 knockout mouse revealed that B cell-derived IL-10 nonredundantly decreases virus-specific CD8(+) T cell responses and plasma cell expansion during murine cytomegalovirus infection and modestly restrains immune activation after challenge with foreign Abs to IgD. In contrast, no role for B cell-derived IL-10 was evident during endotoxemia; however, although B cells dominated lymphoid tissue IL-10 production in this model, myeloid cells were dominant in blood and liver. These data suggest that B cells are an underappreciated source of counter-regulatory IL-10 production in lymphoid tissues, provide a clear rationale for testing the biological role of B cell-derived IL-10 in infectious and inflammatory disease, and underscore the utility of cell type-specific knockouts for mechanistic limning of immune counter-regulation. | lld:pubmed |
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| pubmed-article:19620304 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19620304 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19620304 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:19620304 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19620304 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19620304 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:19620304 | pubmed:author | pubmed-author:MüllerWernerW | lld:pubmed |
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| pubmed-article:19620304 | pubmed:author | pubmed-author:WaismanAriA | lld:pubmed |
| pubmed-article:19620304 | pubmed:author | pubmed-author:KhodounMaratM | lld:pubmed |
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| pubmed-article:19620304 | pubmed:author | pubmed-author:GuYuanyuanY | lld:pubmed |
| pubmed-article:19620304 | pubmed:author | pubmed-author:Surianarayana... | lld:pubmed |
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| pubmed-article:19620304 | pubmed:author | pubmed-author:GrewelingMari... | lld:pubmed |
| pubmed-article:19620304 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19620304 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:19620304 | pubmed:volume | 183 | lld:pubmed |
| pubmed-article:19620304 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19620304 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19620304 | pubmed:pagination | 2312-20 | lld:pubmed |
