Premium
CD4 + T‐cell proliferation responses to wheat polypeptide stimulation in children at different stages of type 1 diabetes autoimmunity
Author(s) -
Hamari Susanna,
Kirveskoski Tiina,
Glumoff Virpi,
Kulmala Petri,
Simell Olli,
Knip Mikael,
Ilonen Jorma,
Veijola Riitta
Publication year - 2015
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/pedi.12256
Subject(s) - autoimmunity , medicine , type 1 diabetes , stimulation , diabetes mellitus , cell growth , immunology , endocrinology , immune system , biochemistry , biology
Aims Our aim was to study whether immune responses to wheat‐based proteins are related to the development of type 1 diabetes. Methods We analysed proliferative T‐cell responses after in vitro gliadin, gluten, whole wheat, and tetanus toxoid stimulation with a carboxyfluorescein succinimidyl ester ( CFSE ) based T‐cell proliferation assay in children at various phases of type 1 diabetes autoimmunity and in healthy autoantibody‐negative control children. Results At an early stage of beta cell autoimmunity the strength and frequencies of positive proliferation responses to gliadin, gluten, and whole wheat did not differ between newly seroconverted children positive for one islet autoantibody and the controls. However, in prediabetic children with at least two islet autoantibodies and also in children with newly diagnosed type 1 diabetes positive T‐cell responses to gliadin were significantly less frequent and the strength of gliadin responses was reduced when compared to the controls. No differences were seen in T‐cell responses to wheat‐based antigens when comparing children with long‐lasting type 1 diabetes with healthy controls. Conclusions/Interpretation Decreased in vitro T‐cell responses to wheat‐based antigens were observed in children with multiple islet autoantibodies and in those with newly diagnosed type 1 diabetes, probably reflecting a generally aberrant immune response during the development of type 1 diabetes.