| pubmed-article:19027331 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19027331 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:19027331 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
| pubmed-article:19027331 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19027331 | pubmed:dateCreated | 2009-2-9 | lld:pubmed |
| pubmed-article:19027331 | pubmed:abstractText | The development of some autoimmune diseases is increasing in the developed world faster than can be accounted for by genetic change. The development of these autoimmune diseases, such as Type 1 diabetes, is known to be influenced by both genetic and environmental factors. Environmental factors which have been considered to play a role include infectious agents such as viruses or bacteria. The search for a common initiating infection in the aetiology of Type 1 diabetes as proved thus far inconclusive. An alternative way of considering a role for infection is that infection may have historically prevented the development of autoimmune disease. In the developing world changes have occurred such that many chronic infections have been eliminated and this may have led to the emergence of autoimmune pathology. Evidence in support of this hypothesis is considered here and factors governing the development of autoimmunity compared with those which might have influenced the development of childhood leukaemia. | lld:pubmed |
| pubmed-article:19027331 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19027331 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19027331 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19027331 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19027331 | pubmed:issn | 1096-0961 | lld:pubmed |
| pubmed-article:19027331 | pubmed:author | pubmed-author:CookeAnneA | lld:pubmed |
| pubmed-article:19027331 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19027331 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:19027331 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19027331 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19027331 | pubmed:pagination | 105-7 | lld:pubmed |
| pubmed-article:19027331 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:19027331 | pubmed:meshHeading | pubmed-meshheading:19027331... | lld:pubmed |
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| pubmed-article:19027331 | pubmed:meshHeading | pubmed-meshheading:19027331... | lld:pubmed |
| pubmed-article:19027331 | pubmed:articleTitle | Infection and autoimmunity. | lld:pubmed |
| pubmed-article:19027331 | pubmed:affiliation | Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, UK. ac@mole.bio.cam.ac.uk | lld:pubmed |
| pubmed-article:19027331 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19027331 | pubmed:publicationType | Review | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19027331 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19027331 | lld:pubmed |
