| pubmed-article:17523948 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17523948 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:17523948 | lifeskim:mentions | umls-concept:C0271737 | lld:lifeskim |
| pubmed-article:17523948 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:17523948 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:17523948 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17523948 | pubmed:dateCreated | 2007-5-25 | lld:pubmed |
| pubmed-article:17523948 | pubmed:abstractText | Polymorphisms in the low-affinity Fcgamma receptors (FcgammaR) modulate their capacity to bind IgG and the subsequent immune response. Different FcgammaR polymorphisms have been reported to be associated with susceptibility and severity of various autoimmune diseases. We wanted to investigate associations between FcgammaR polymorphisms and autoimmune primary adrenal failure (Addison's disease). We have genotyped 149 patients with Addison's disease and 89 healthy controls for common polymorphisms in the genes coding for FcgammaRIIa, FcgammaRIIIa and FcgammaRIIIb using polymerase chain reaction. Patients with Addison's disease and controls showed no differences in genotype distributions of FcgammaRIIa, FcgammaRIIIa and FcgammaRIIIb. The results indicate that different FcgammaR polymorphisms do not have an impact on immune responses involved in the development of autoimmune Addison's disease. | lld:pubmed |
| pubmed-article:17523948 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17523948 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17523948 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17523948 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17523948 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17523948 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17523948 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17523948 | pubmed:issn | 0300-9475 | lld:pubmed |
| pubmed-article:17523948 | pubmed:author | pubmed-author:VedelerC ACA | lld:pubmed |
| pubmed-article:17523948 | pubmed:author | pubmed-author:HusebyeE SES | lld:pubmed |
| pubmed-article:17523948 | pubmed:author | pubmed-author:MyhrK-MKM | lld:pubmed |
| pubmed-article:17523948 | pubmed:author | pubmed-author:WolffA S BAS | lld:pubmed |
| pubmed-article:17523948 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17523948 | pubmed:volume | 65 | lld:pubmed |
| pubmed-article:17523948 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17523948 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17523948 | pubmed:pagination | 555-8 | lld:pubmed |
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| pubmed-article:17523948 | pubmed:meshHeading | pubmed-meshheading:17523948... | lld:pubmed |
| pubmed-article:17523948 | pubmed:meshHeading | pubmed-meshheading:17523948... | lld:pubmed |
| pubmed-article:17523948 | pubmed:meshHeading | pubmed-meshheading:17523948... | lld:pubmed |
| pubmed-article:17523948 | pubmed:meshHeading | pubmed-meshheading:17523948... | lld:pubmed |
| pubmed-article:17523948 | pubmed:meshHeading | pubmed-meshheading:17523948... | lld:pubmed |
| pubmed-article:17523948 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17523948 | pubmed:articleTitle | Fc-gamma receptor polymorphisms are not associated with autoimmune Addison's disease. | lld:pubmed |
| pubmed-article:17523948 | pubmed:affiliation | Institute of Medicine, University of Bergen, Bergen, Norway. | lld:pubmed |
| pubmed-article:17523948 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17523948 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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