pubmed-article:19383625 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0024264 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0237753 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C1427306 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:19383625 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
pubmed-article:19383625 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:19383625 | pubmed:dateCreated | 2009-7-7 | lld:pubmed |
pubmed-article:19383625 | pubmed:abstractText | The novel coinhibitory receptor BTLA may have a regulatory role in maintaining peripheral tolerance; however, its role in autoimmune diabetes is unknown. In this study, we show that anti-BTLA mAb 6F7 selectively depleted pathogenic B and CD4+ T(H) cells; enhanced the proportion of cells with the forkhead box p3+ PD-1+CD4+ regulatory T phenotype; and increased the production of potentially protective (IL-10) and detrimental (IL-2, IFN-gamma) cytokines in NOD mice. As interactions between BTLA and PD-1 coinhibitory pathways have been described in the cardiac allograft model, we also investigated if these pathways may have significant interaction in autoimmune diabetes. Anti-BTLA inhibited anti-PD-1-potentiated total IL-12 (p40+p70) production, suggesting the possibility that anti-BTLA may have a greater effect in the setting of anti-PD-1-triggered diabetes. To test this, NOD mice at 4 and 10 weeks of age were treated with anti-BTLA mAb, anti-PD-1 mAb, both mAb, or isotype control and were monitored for diabetes development. Although anti-BTLA mAb delayed diabetes onset significantly in 10- but not 4-week-old NOD mice, anti-BTLA mAb attenuated anti-PD-1-induced diabetes in both age groups. Hence, strategies targeting BTLA+ lymphocytes or therapies enhancing the BTLA-negative cosignal may prove valuable in treating autoimmune diabetes. | lld:pubmed |
pubmed-article:19383625 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:language | eng | lld:pubmed |
pubmed-article:19383625 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19383625 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19383625 | pubmed:month | Jul | lld:pubmed |
pubmed-article:19383625 | pubmed:issn | 1938-3673 | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:HancockWayne... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:MurphyKenneth... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:ShapiroA M... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:MeraniShaheed... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:TruongWayneW | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:RaynerDavid... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:AndersonColin... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:PlesterJennif... | lld:pubmed |
pubmed-article:19383625 | pubmed:author | pubmed-author:ThangaveluGov... | lld:pubmed |
pubmed-article:19383625 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19383625 | pubmed:volume | 86 | lld:pubmed |
pubmed-article:19383625 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19383625 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19383625 | pubmed:pagination | 41-51 | lld:pubmed |
pubmed-article:19383625 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:19383625 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19383625 | pubmed:articleTitle | BTLA targeting modulates lymphocyte phenotype, function, and numbers and attenuates disease in nonobese diabetic mice. | lld:pubmed |
pubmed-article:19383625 | pubmed:affiliation | Surgical Medical Research Institute, Department of Surgery, Faculty of Medicine, University of Alberta, Edmonton, Alberta, Canada. | lld:pubmed |
pubmed-article:19383625 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19383625 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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