title: Anti-insulin activity in normal newborn cord-blood serum: absence of IgG-mediated insulin binding.
abstract: Insulin autoantibodies (IAAs) are present in approximately 60% of type I diabetes patients at onset and are used as predictors for the disease. Although the prevalence of IAAs in the general population has been reported to be <1%, preliminary data have pointed out a higher proportion of IAA positivity in newborn cord-blood serum, and some authors have suggested that they are immunoglobulin G antibodies, resulting from a hypothetical gestational insulitis. To characterize this insulin-binding activity, we analyzed cord-blood sera from 100 healthy newborns, as well as serum from 21 of their mothers at delivery, 179 new-onset type I diabetic patients, and 200 healthy control subjects. IAAs were present in 0.5% of the control subjects and 54% of new-onset type I diabetic patients. On the other hand, 96% of the newborn cord-blood sera showed anti-insulin activity, while it was detected in only 14% of their mothers. No significant differences were observed between cord sera and the general population for islet-cell or anti-GAD autoantibodies. Anti-insulin activity in cord serum was not bound by protein A or protein G, in contrast with type I diabetes-related IAA activity. We conclude that this insulin-binding activity, present in most newborn cord sera and specific to the child, is not IgG mediated. These data, together with the absence of other pancreatic autoimmunity markers in this population, suggest that it is an isolated phenomenon not related to type I diabetes or other pancreatic autoimmune processes and is due to the presence of a cross-reacting molecule in cord blood that has yet to be identified.
authors.affiliation: Department of Pediatrics, Hospital de Cruces, Barakaldo-Basque Country, Bizkaia, Spain.
authors.forename: J R
authors.initials: JR
authors.lastname: Bilbao
authors.forename: B
authors.initials: B
authors.lastname: Calvo
authors.forename: I
authors.initials: I
authors.lastname: Urrutia
authors.forename: A
authors.initials: A
authors.lastname: Linares
authors.forename: L
authors.initials: L
authors.lastname: Castaño
mesh_terms: D000293:Adolescent; D000328:Adult; D000375:Aging / Q000276:immunology / Q000378:metabolism; D001323:Autoantibodies / Q000097:blood; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000196:embryology / Q000276:immunology; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007328:Insulin / Q000378:metabolism; D007330:Insulin Antibodies / Q000097:blood* / Q000378:metabolism; D007515:Islets of Langerhans / Q000276:immunology; D008875:Middle Aged
chemical_list: D001323:Autoantibodies; D007328:Insulin; D007330:Insulin Antibodies; C024211:islet cell antibody; D005968:Glutamate Decarboxylase