| pubmed-article:20624892 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20624892 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:20624892 | lifeskim:mentions | umls-concept:C0887899 | lld:lifeskim |
| pubmed-article:20624892 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
| pubmed-article:20624892 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:20624892 | lifeskim:mentions | umls-concept:C1420816 | lld:lifeskim |
| pubmed-article:20624892 | lifeskim:mentions | umls-concept:C0443211 | lld:lifeskim |
| pubmed-article:20624892 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:20624892 | pubmed:dateCreated | 2010-8-3 | lld:pubmed |
| pubmed-article:20624892 | pubmed:abstractText | Autoimmunity is traditionally attributed to altered lymphoid cell selection and/or tolerance, whereas the contribution of innate immune cells is less well understood. Autoimmunity is also associated with increased levels of B cell-activating factor of the TNF family (BAFF; also known as B lymphocyte stimulator), a cytokine that promotes survival of self-reactive B cell clones. We describe an important role for myeloid cells in autoimmune disease progression. Using Lyn-deficient mice, we show that overproduction of BAFF by hyperactive myeloid cells contributes to inflammation and autoimmunity in part by acting directly on T cells to induce the release of IFN-gamma. Genetic deletion of IFN-gamma or reduction of BAFF activity, achieved by either reducing myeloid cell hyperproduction or by treating with an anti-BAFF monoclonal antibody, reduced disease development in lyn(-/-) mice. The increased production of IFN-gamma in lyn(-/-) mice feeds back on the myeloid cells to further stimulate BAFF release. Expression of BAFF receptor on T cells was required for their full activation and IFN-gamma release. Overall, our data suggest that the reciprocal production of BAFF and IFN-gamma establishes an inflammatory loop between myeloid cells and T cells that exacerbates autoimmunity in this model. Our findings uncover an important pathological role of BAFF in autoimmune disorders. | lld:pubmed |
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| pubmed-article:20624892 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20624892 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20624892 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20624892 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20624892 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:20624892 | pubmed:issn | 1540-9538 | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:LowellCliffor... | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:CassatellaMar... | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:ChuChing-Lian... | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:ScapiniPatriz... | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:MigoneThi-Sau... | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:HuYongmeiY | lld:pubmed |
| pubmed-article:20624892 | pubmed:author | pubmed-author:DefrancoAntho... | lld:pubmed |
| pubmed-article:20624892 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20624892 | pubmed:day | 2 | lld:pubmed |
