| pubmed-article:19349693 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19349693 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:19349693 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:19349693 | lifeskim:mentions | umls-concept:C0017668 | lld:lifeskim |
| pubmed-article:19349693 | lifeskim:mentions | umls-concept:C0108793 | lld:lifeskim |
| pubmed-article:19349693 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19349693 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:19349693 | pubmed:dateCreated | 2009-5-6 | lld:pubmed |
| pubmed-article:19349693 | pubmed:abstractText | Heritable and acquired diseases of podocytes can result in focal and segmental glomerulosclerosis (FSGS). We modeled FSGS by passively transferring mouse podocyte-specific sheep Abs into BALB/c mice. BALB/c mice deficient in the key complement regulator, decay-accelerating factor (DAF), but not WT or CD59-deficient BALB/c mice developed histological and ultrastructural features of FSGS, marked albuminuria, periglomerular monocytic and T cell inflammation, and enhanced T cell reactivity to sheep IgG. All of these findings, which are characteristic of FSGS, were substantially reduced by depleting CD4+ T cells from Daf(-/-) mice. Furthermore, WT kidneys transplanted into Daf(-/-) recipients and kidneys of DAF-sufficient but T cell-deficient Balb/(cnu/nu) mice reconstituted with Daf(-/-) T cells developed FSGS. In contrast, DAF-deficient kidneys in WT hosts and Balb/(cnu/nu) mice reconstituted with DAF-sufficient T cells did not develop FSGS. Thus, we have described what we believe to be a novel mouse model of FSGS attributable to DAF-deficient T cell immune responses. These findings add to growing evidence that complement-derived signals shape T cell responses, since T cells that recognize sheep Abs bound to podocytes can lead to cellular injury and development of FSGS. | lld:pubmed |
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| pubmed-article:19349693 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19349693 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19349693 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19349693 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19349693 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19349693 | pubmed:month | May | lld:pubmed |
| pubmed-article:19349693 | pubmed:issn | 1558-8238 | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:ZhangJianJ | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:WangYingY | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:ShanklandStua... | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:PippinJeffrey... | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:HaasMarkM | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:BaoLihuaL | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:QuiggRichard... | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:AlpersCharles... | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:QiaoGuilinG | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:MiwaTakashiT | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:SongWen-ChaoW... | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:MintoAndrew... | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:ChangAnthonyA | lld:pubmed |
| pubmed-article:19349693 | pubmed:author | pubmed-author:PetkovaMiglen... | lld:pubmed |
