pubmed-article:19079673 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19079673 | lifeskim:mentions | umls-concept:C0022658 | lld:lifeskim |
pubmed-article:19079673 | lifeskim:mentions | umls-concept:C0039198 | lld:lifeskim |
pubmed-article:19079673 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:19079673 | pubmed:dateCreated | 2008-12-16 | lld:pubmed |
pubmed-article:19079673 | pubmed:abstractText | Regulatory T cells (Tregs) have a key role in immune homeostasis and in suppressing unwanted inflammatory responses toward self-antigens. Tregs have been implicated in the control of initial activation events, and play roles in limiting proliferation, differentiation and effector functions of T helper cells. However, the activities of Tregs in the development and progression of kidney disease are not fully elucidated. We have demonstrated the potency of Tregs in animal models of kidney disease. In this review, we summarise mechanistic information from rodent models on the roles of Tregs in glomerular immunopathology and discuss the function of Tregs in diverse kidney diseases. Further studies of Tregs should provide important insights into designing of therapeutic strategies to prevent human kidney disease. | lld:pubmed |
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pubmed-article:19079673 | pubmed:language | eng | lld:pubmed |
pubmed-article:19079673 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19079673 | pubmed:status | PubMed-not-MEDLINE | lld:pubmed |
pubmed-article:19079673 | pubmed:issn | 1940-5901 | lld:pubmed |
pubmed-article:19079673 | pubmed:author | pubmed-author:KobAA | lld:pubmed |
pubmed-article:19079673 | pubmed:author | pubmed-author:WangYipingY | lld:pubmed |