pubmed-article:16778988 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16778988 | lifeskim:mentions | umls-concept:C0962189 | lld:lifeskim |
pubmed-article:16778988 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:16778988 | lifeskim:mentions | umls-concept:C0024426 | lld:lifeskim |
pubmed-article:16778988 | lifeskim:mentions | umls-concept:C1523987 | lld:lifeskim |
pubmed-article:16778988 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:16778988 | pubmed:dateCreated | 2006-7-6 | lld:pubmed |
pubmed-article:16778988 | pubmed:abstractText | The IL-21 receptor (IL-21R) shows significant homology with the IL-4R, and CD4+ Th2 cells are an important source of IL-21. Here we examined whether the IL-21R regulates the development of Th2 responses in vivo. To do this, we infected IL-21R-/- mice with the Th2-inducing pathogens Schistosoma mansoni and Nippostrongylus brasiliensis and examined the influence of IL-21R deficiency on the development of Th2-dependent pathology. We showed that granulomatous inflammation and liver fibrosis were significantly reduced in S. mansoni-infected IL-21R-/- mice and in IL-21R+/+ mice treated with soluble IL-21R-Fc (sIL-21R-Fc). The impaired granulomatous response was also associated with a marked reduction in Th2 cytokine expression and function, as evidenced by the attenuated IL-4, IL-13, AMCase, Ym1, and FIZZ1 (also referred to as RELMalpha) responses in the tissues. A similarly impaired Th2 response was observed following N. brasiliensis infection. In vitro, IL-21 significantly augmented IL-4Ralpha and IL-13Ralpha1 expression in macrophages, resulting in increased FIZZ1 mRNA and arginase-1 activity following stimulation with IL-4 and IL-13. As such, these data identify the IL-21R as an important amplifier of alternative macrophage activation. Collectively, these results illustrate an essential function for the IL-21R in the development of pathogen-induced Th2 responses, which may have relevance in therapies for both inflammatory and chronic fibrotic diseases. | lld:pubmed |
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pubmed-article:16778988 | pubmed:language | eng | lld:pubmed |
pubmed-article:16778988 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16778988 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:16778988 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16778988 | pubmed:month | Jul | lld:pubmed |
pubmed-article:16778988 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:GrusbyMichael... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:WynnThomas... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:CollinsMaryM | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:ThompsonRober... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:CheeverAllen... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:UrbanJoseph... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:YoungDeborah... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:PesceJohnJ | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:KaviratneMall... | lld:pubmed |
pubmed-article:16778988 | pubmed:author | pubmed-author:RamalingamThi... | lld:pubmed |
pubmed-article:16778988 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16778988 | pubmed:volume | 116 | lld:pubmed |
pubmed-article:16778988 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16778988 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16778988 | pubmed:pagination | 2044-55 | lld:pubmed |
pubmed-article:16778988 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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