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CpG oligodeoxynucleotides accelerate reovirus type 2‐triggered insulitis in DBA/1 suckling mice
Author(s) -
Hayashi T.,
Yoshinaka K.,
Hasegawa K.,
Maeda K.,
Onodera T.
Publication year - 2002
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1046/j.1365-2613.2003.00231.x
Subject(s) - insulitis , cpg oligodeoxynucleotide , cpg site , nod , nod mice , pancreatic islets , immunology , islet , cd8 , autoimmunity , biology , interferon , interferon gamma , autoantibody , cytokine , immune system , endocrinology , antibody , insulin , diabetes mellitus , gene , biochemistry , gene expression , dna methylation
Summary. We reported previously that reovirus type‐2 (Reo‐2) triggers T‐helper (Th) 1‐mediated autoimmune insulitis resulting in temporal impaired glucose tolerance (IGT) approximately 10 days post infection (d.p.i) in suckling DBA/1 mice. We hypothesized that CpG motifs in bacteria may enhance virus‐induced insulitis through its content of unmethylated CpG motifs. In the infected mice, the intraperitoneal treatment of synthetic 20‐base oligodeoxynucleotides with CpG motifs (CpG ODN) caused increase in cumulative incidence of insulitis with IGT, increased serum interferon (IFN)‐γ concentration, and high frequency of autoantibody against pancreatic islet cells, compared to the infected mice without CpG ODN at 17 d.p.i. Also CD4 + and CD8 + lymphocytes infiltrated in and/or around pancreatic islets in the CpG ODN‐treated mice. This evidence suggests that CpG ODN may contribute to accelerate Reo‐2‐induced autoimmune reaction against pancreatic islet cells via additional effects of Th1 cytokines especially IFN‐γ.