The ABBOS-peptide from bovine serum albumin causes an IFN-γ and IL-4 mRNA response in lymphocytes from children with recent onset of type 1 diabetes
2000 (English)In: Diabetes Research and Clinical Practice, ISSN 0168-8227, E-ISSN 1872-8227, Vol. 47, no 3, 199-207 p.Article in journal (Refereed) Published
The ABBOS-peptide from bovine serum albumin (BSA) in cow’s milk has been suggested to initiate the autoimmune process against the β-cells leading to type 1 diabetes. The aim of this study was to elucidate if the ABBOS-peptide is a possible trigger of type 1 diabetes. The cytokines IL-4 and IFN-γ were determined at the level of transcription as mRNA in lymphocytes, stimulated with the ABBOS-peptide. Sixteen children with newly diagnosed type 1 diabetes were compared with 10 healthy controls matched for the diabetes associated HLA-type DR3/4. Antibodies to bovine serum albumin (BSA), insulin antibodies (IA), and antibodies against islet cells (ICA) were determined, as well as serum C-peptide. Increased mRNA expression for IFN-γ and/or IL-4 could be observed in lymphocytes from 13/16 children with recent onset of diabetes after in vitro stimulation with the ABBOS-peptide. Low expression of IFN-γ mRNA was associated with high secretion of C-peptide, whereas a positive relationship could be observed between expression of IL-4 mRNA and insulin antibodies. Expression of IFN-γ and/or IL-4 mRNA was also detected in lymphocytes from 6/10 healthy controls. ABBOS may have a role as a reactive epitope in the upregulation of the autoimmune process against the β-cells but ABBOS does not seem to cause any specific Th1 response. An increased mRNA expression could also be seen in lymphocytes from healthy controls. Thus, the ABBOS-peptide might just cause or reflect an unspecific immune activity.
Place, publisher, year, edition, pages
2000. Vol. 47, no 3, 199-207 p.
ABBOS, IFN-γ, IL-4, Type 1 diabetes, Th-lymphocytes
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-25986DOI: 10.1016/S0168-8227(99)00127-8Local ID: 10438OAI: oai:DiVA.org:liu-25986DiVA: diva2:246534