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Enhanced levels of cow’s milk antibodies in infancy in children who develop type 1 diabetes later in childhood
Author(s) -
Luopajärvi Kristiina,
Savilahti Erkki,
Virtanen Suvi M,
Ilonen Jorma,
Knip Mikael,
Åkerblom Hans K,
Vaarala Outi
Publication year - 2008
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1111/j.1399-5448.2008.00413.x
Subject(s) - medicine , autoantibody , type 1 diabetes , antibody , immunology , diabetes mellitus , immune system , pathogenesis , antigen , insulin , endocrinology
Background: Early exposure to cow’s milk (CM) proteins have been implicated in the pathogenesis of type 1 diabetes (T1D). Objective: We analyzed the development of the humoral immune response to dietary CM proteins in early childhood and its relation to later T1D. Subjects and methods: We studied a subgroup of 94 children randomized to be weaned to a CM‐based infant formula in the trial to reduce insulin‐dependent diabetes mellitus in the genetically at risk (TRIGR) pilot study. All subjects carried human leukocyte antigen‐conferred T1D susceptibility and had an affected first‐degree relative. After 7 years of follow‐up, 8 subjects had progressed to T1D, 15 had at least one disease‐associated autoantibody, and 71 remained autoantibody negative (controls). Immunoglobulin (Ig) G and IgA class antibodies to whole CM formula, beta‐lactoglobulin (BLG), bovine serum albumin, and alpha‐casein and IgG antibodies to bovine insulin (BI) were measured with enzyme‐linked immunosorbent assays from sequential samples. Results: The children with later T1D showed increased IgG levels to BLG from 3 to 18 months of age (p = 0.028) and enhanced IgA levels to CM formula at the age of 9 months (p = 0.022) compared with controls. In the children with an affected father or sibling, IgG antibodies to BI were higher in autoantibody‐positive subjects than in autoantibody‐negative subjects at 18 months of age (p = 0.022). Conclusion: An enhanced humoral immune response to various CM proteins in infancy is seen in a subgroup of those children who later progress to T1D. Accordingly, a dysregulated immune response to oral antigens is an early event in the pathogenesis of T1D.