| pubmed-article:19542376 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0024501 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0384648 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0200633 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C1825592 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C1424252 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C1705097 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C1705947 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:19542376 | lifeskim:mentions | umls-concept:C0721534 | lld:lifeskim |
| pubmed-article:19542376 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19542376 | pubmed:dateCreated | 2009-7-7 | lld:pubmed |
| pubmed-article:19542376 | pubmed:abstractText | G-CSF, its receptor, and IL-17 receptor A (IL-17RA) are all required to maintain baseline neutrophil counts in mice. In this study, we tested whether IL-17F could compensate and maintain baseline neutrophil counts in the absence of IL-17A. Unlike the reduced neutrophil counts found in IL-17RA-deficient mice, neutrophil counts were mildly increased in IL-17A-deficient (Il17a(-/-)) animals. There was no evidence for infection or altered neutrophil function. Plasma G-CSF and IL-17F levels were elevated in Il17a(-/-) compared with wild-type mice. IL-17F was mainly produced in the spleen and mesenteric lymph nodes, but IL-23 was unaltered in Il17a(-/-) mice. Instead, Il17a(-/-) splenocytes differentiated with IL-6, TGF-beta, and IL-23 ex vivo produced significantly more IL-17F in response to IL-23 than wild-type cells. Adding rIL-17A to Il17a(-/-) splenocyte cultures reduced IL-17F mRNA and protein secretion. These effects were also observed in wild-type but not IL-17RA-deficient cells. We conclude that IL-17A mediated suppression of IL-17F production and secretion requires IL-17RA and is relevant to maintain the normal set point of blood neutrophil counts in vivo. | lld:pubmed |
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| pubmed-article:19542376 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19542376 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19542376 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:19542376 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19542376 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19542376 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:19542376 | pubmed:author | pubmed-author:LeyKlausK | lld:pubmed |
| pubmed-article:19542376 | pubmed:author | pubmed-author:von... | lld:pubmed |
| pubmed-article:19542376 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19542376 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:19542376 | pubmed:volume | 183 | lld:pubmed |
| pubmed-article:19542376 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19542376 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19542376 | pubmed:pagination | 865-73 | lld:pubmed |
| pubmed-article:19542376 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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