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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1999-1-14
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1120544,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1285060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1357775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1556180,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1574800,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1864485,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1936620,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1936622,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1946445,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1967440,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-1985125,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-2197139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-2204345,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-3066606,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-6118756,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-6363172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-7537670,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-7539034,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-7690836,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-7773291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-7962558,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-8098789,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-8247037,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-8612195,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-8621013,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-8772714,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-9088889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-9118783,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-9165225,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-9376075,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-9401639,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9844045-9662050
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
114
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
370-6
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9844045-Adolescent,
pubmed-meshheading:9844045-Adult,
pubmed-meshheading:9844045-Alleles,
pubmed-meshheading:9844045-Antibody Formation,
pubmed-meshheading:9844045-Autoantigens,
pubmed-meshheading:9844045-Autoimmunity,
pubmed-meshheading:9844045-Child,
pubmed-meshheading:9844045-Child, Preschool,
pubmed-meshheading:9844045-Diabetes Mellitus, Type 1,
pubmed-meshheading:9844045-Female,
pubmed-meshheading:9844045-HLA-DR3 Antigen,
pubmed-meshheading:9844045-HLA-DR4 Antigen,
pubmed-meshheading:9844045-Humans,
pubmed-meshheading:9844045-Immunity, Cellular,
pubmed-meshheading:9844045-Infant,
pubmed-meshheading:9844045-Insulin,
pubmed-meshheading:9844045-Islets of Langerhans,
pubmed-meshheading:9844045-Male,
pubmed-meshheading:9844045-Middle Aged,
pubmed-meshheading:9844045-Minisatellite Repeats
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pubmed:year |
1998
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pubmed:articleTitle |
Autoimmune responses to the beta cell autoantigen, insulin, and the INS VNTR-IDDM2 locus.
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pubmed:affiliation |
Departments of Internal Medicine, Instituto Scientifico San Raffaele, Milan, Italy.
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pubmed:publicationType |
Journal Article
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