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Publication : IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse.

First Author  Balasa B Year  2000
Journal  Cell Immunol Volume  202
Issue  2 Pages  97-102
PubMed ID  10896769 Mgi Jnum  J:114170
Mgi Id  MGI:3688457 Doi  10.1006/cimm.2000.1658
Citation  Balasa B, et al. (2000) IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse. Cell Immunol 202(2):97-102
abstractText  IL-10 exterts profound immunostimulatory and immunoinhibitory effects. To explore the role of IL-10 in autoimmune diabetes of nonobese diabetic (NOD) mice, we generated IL-10-deficient NOD mice. In contrast to our previous results with neutralizing antibodies to IL-10, IL-10-deficient NOD mice developed insulitis and their splenocytes readily responded to islet antigen glutamic acid decarboxylase 65. IL-10-deficient NOD mice did not develop accelerated spontaneous diabetes. On the other hand, IL-10-deficient NOD mice developed accelerated disease following cyclophosphamide (CYP) injection. These findings demonstrate that IL-10 is dispensable for autoimmune diabetes. IL-10's absence fails to accelerate endogenous diabetes but potentiates CYP-induced diabetes.
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