@article{oai:nagasaki-u.repo.nii.ac.jp:00016888,
 author = {Fukushima, Keiko and Abiru, Norio and Nagayama, Yuji and Kobayashi, Masakazu and Satoh, Tsuyoshi and Nakahara, Mami and Kawasaki, Eiji and Yamasaki, Hironori and Ueha, Satoshi and Matsushima, Koji and Liu, Edwin and Eguchi, Katsumi},
 issue = {4},
 journal = {Biochemical and biophysical research communications},
 month = {Mar},
 note = {Insulin peptide B:9-23 is a major autoantigen in type 1 diabetes. Combined treatment with B:9-23 peptide and polyinosinic-polycytidylic acid (poly I:C), but neither alone, induce insulitis in normal BALB/c mice. In contrast, the combined treatment accelerated insulitis, but prevented diabetes in NOD mice. Our immunofluorescence study with anti-CD4/anti-Foxp3 revealed that the proportion of Foxp3 positive CD4(+)CD25(+) regulatory T cells (Tregs) was elevated in the islets of NOD mice treated with B:9-23 peptide and poly I:C, as compared to non-treated mice. Depletion of Tregs by anti-CD25 antibody hastened spontaneous development of diabetes in non-treated NOD mice, and abolished the protective effect of the combined treatment and conversely accelerated the onset of diabetes in the treated mice. These results indicate that poly I:C combined with B:9-23 peptide promotes infiltration of both pathogenic T cells and predominantly Tregs into the islets, thereby inhibiting progression from insulitis to overt diabetes in NOD mice., Biochemical and biophysical research communications, 367(4), pp.719-724; 2008},
 pages = {719--724},
 title = {Combined insulin B:9-23 self-peptide and polyinosinic-polycytidylic acid accelerate insulitis but inhibit development of diabetes by increasing the proportion of CD4+Foxp3+ regulatory T cells in the islets in non-obese diabetic mice.},
 volume = {367},
 year = {2008}
}