| pubmed-article:9844045 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C1708726 | lld:lifeskim |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C0004359 | lld:lifeskim |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C1337112 | lld:lifeskim |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C0004366 | lld:lifeskim |
| pubmed-article:9844045 | lifeskim:mentions | umls-concept:C1516518 | lld:lifeskim |
| pubmed-article:9844045 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9844045 | pubmed:dateCreated | 1999-1-14 | lld:pubmed |
| pubmed-article:9844045 | pubmed:abstractText | Type 1 diabetes is associated with autoimmunity to insulin. Genetic susceptibility to type 1 diabetes is polygenic and includes the INS VNTR-IDDM2 locus which may regulate the expression of insulin in pancreas and thymus. In order to determine whether insulin autoimmunity could be attributed to a genetic susceptibility conferred by the INS VNTR-IDDM2 locus, peripheral blood T cell proliferation to human insulin and insulin autoantibodies (IAA) was measured in patients with new onset type 1 diabetes and control subjects. IAA were detected in 21 of 53 patients and in none of 25 control subjects, while T cell responses were low (stimulation index range 0.4-7.2) and similar in both groups. Both antibody and T cell responses were higher in younger subjects and IAA were more prevalent in patients with the HLA-DR4 allele. No relationship was observed between humoral and cellular responses to insulin. No association was found between the INS VNTR-IDDM2-susceptible allele and insulin autoimmunity. Increased T cell responses and IAA were found in patients with either the diabetes-susceptible or the diabetes-protective INS VNTR-IDDM2 locus genotypes, and increased T cell responses were also found in control subjects with either susceptible or protective INS VNTR-IDDM2 locus genotypes. This study confirms that primary T cell proliferative responses to insulin are low and detectable also in control subjects. The detection of T cell proliferation and autoantibodies to insulin in subjects with and without the protective INS VNTR-IDDM2 locus genotypes does not support the hypothesis of an allele-specific capacity for tolerance induction which could determine a susceptibility to develop autoimmunity against the insulin protein and subsequently diabetes. | lld:pubmed |
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| pubmed-article:9844045 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9844045 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9844045 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9844045 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9844045 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:9844045 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:9844045 | pubmed:author | pubmed-author:BelloniCC | lld:pubmed |
| pubmed-article:9844045 | pubmed:author | pubmed-author:MeschiFF | lld:pubmed |
| pubmed-article:9844045 | pubmed:author | pubmed-author:PastoreM RMR | lld:pubmed |
| pubmed-article:9844045 | pubmed:author | pubmed-author:BonifacioEE | lld:pubmed |
| pubmed-article:9844045 | pubmed:author | pubmed-author:DozioNN | lld:pubmed |
| pubmed-article:9844045 | pubmed:author | pubmed-author:SarugeriEE | lld:pubmed |
| pubmed-article:9844045 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9844045 | pubmed:volume | 114 | lld:pubmed |
| pubmed-article:9844045 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9844045 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9844045 | pubmed:pagination | 370-6 | lld:pubmed |
| pubmed-article:9844045 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:9844045 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9844045 | pubmed:articleTitle | Autoimmune responses to the beta cell autoantigen, insulin, and the INS VNTR-IDDM2 locus. | lld:pubmed |
| pubmed-article:9844045 | pubmed:affiliation | Departments of Internal Medicine, Instituto Scientifico San Raffaele, Milan, Italy. | lld:pubmed |
| pubmed-article:9844045 | pubmed:publicationType | Journal Article | lld:pubmed |
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