International Immunology, Vol. 12, No. 7, 1075-1083,
July 2000
© 2000 Japanese Society for Immunology
Suppression of insulitis and diabetes in B cell-deficient mice treated with streptozocin: B cells are essential for the TCR clonotype spreading of islet-infiltrating T cells
1 Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences,
2 Department of Medical Technology, School of Health Sciences, and
3 Department of Molecular Immunology, Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan
4 Department of Clinical Medicine, School of Medicine, Fukuoka University, Fukuoka 814-0133, Japan
5 Molecular Analysis Unit, Central Institute for Experimental Animals, Kawasaki 216-0001, Japan
Correspondence to: S. Nagafuchi or S. Kondo, Department of Medical Technology, School of Health Sciences, and the Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
In order to clarify the role of B cells in the development of insulitis and diabetes, B cell-deficient (B–) mice treated with streptozocin (STZ) were studied. The extent of insulitis and the cumulative incidence of diabetes were significantly suppressed in B– mice (P < 0.0001), indicating that B cells are crucial for the progression of insulitis and diabetes. Accumulation of both CD4+ T cells and B cells was observed in islets of B+ mice, while CD4+ T cells but not B cells were found in B– mice. A few CD8+ T cells and macrophages were detectable in both types of mice. The immunohistochemical study did not reveal any change in the subpopulations of infiltrating lymphocytes except for the absence of B cells in the B– mice. TCR Vß gene repertoire usage of islet-infiltrating T cells was restricted to some extent in the B+ or B– mice, but there was no significant difference between the B+ and B– mice, suggesting that the initial islet-reactive T cell response can occur in the absence of B cells. In contrast, TCR clonotype spreading of islet-infiltrating T cells was significantly suppressed in B– mice compared with B+ mice (P < 0.0001). These data suggest that initial priming of T cells is not impaired and TCR Vß repertoire usage is not limited by the lack of B cells, while B cells are important essentially for the spreading of islet-infiltrating clonal T cells in autoimmune diabetic mice induced with STZ.
Keywords: B Lymphocytes, diabetes, insulitis, single-stranded conformation polymorphism, TCR clonotype
Transmitting editor: D. Kitamura
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